Recently there has been some news coverage
on the possible connection of pesticides with the development of autism
spectrum disorders (ASD). While I am thrilled that the connection between
environment and mental health is getting covered, I prefer to read the actual
research to determine what is being found, and how the data was collected.
The literature on pesticides and ASD is
very limited, however what is available is very interesting.
In 2007 Roberts and colleagues published
their findings looking at a potential connection between ASD and exposure to
pesticides. They were specifically interested in pesticides which were
troubling to the area population, as well as those thought to have a negative
effect on health. In total they ended up looking at 54 pesticides.
The study took place in central California
(Roberts et al, 2007). In may ways a study linking autism and pesticide usage
could only be done in California. California is home to the California
Department of Pesticide Regulation which regulates the use and sales of
pesticides (CDPR, 2013). It also has the Regional Center, a division of the Department
of Developmental Services, which provides services to individuals diagnosed, or
at risk of, developmental disabilities (CDDS, 2014). Using information from
these two departments Roberts and colleagues (2007) were able to link pesticide
usage and instances of ASD and then compare pesticide usage with a control
group matched on race/ethnicity, maternal education, and residing in the same
geographic area (defined by the regional center boundaries; Roberts et al,
2007).
The study was specifically interested in
crucial neural development, specifically the first trimester of pregnancy when
the brain is developing (Roberts et al, 2007). To analyze the data researchers
then broke the time periods up into two month increments starting at 300 days
before conception and ending at 300 days after conception, spanning the entire
period of a typical gestational period.
The pesticides containing Organochlorine,
such as dicofol and endosulfan, was significantly related to the occurrence of
ASD within the area of slightly more than one mile (Roberts et al, 2007). It is
only after this radius that the effect of organochlorine in relation to the
development of ASD becomes non-significant. They found that biggest area of
effect was slightly less than a month after conception, following the neural
tube closure, the area that will later develop into the brain (Roberts et al,
2007). Children of mothers who were exposed to organochlorine within this span
of 26-81 days were 7.6 times more likely to later be diagnosed with an ASD
diagnosis (Shelton, Hertz-Picciotto, & Pessah, 2012).
Using the same data and reanalyzing it
using a statistical technique which did not require data to be analyzed using
specific time periods, Roberts and English (2012) replicated the findings in the
previous study and found an additional area of concern after birth when
children were between the ages of 3 to 9 months old (Roberts & English,
2012).
Evidence is continually mounting that
suggests a relationship between pesticide use and the diagnosis of ASD. Shelton
and colleagues (2014) recently released a study looking at pesticide exposure
to mothers in an ongoing Childhood Autism Risks from Genes and Environment
(CHARGE) study, which is also based in California. Instead of using population
based samples, the researchers interacted with over 1,600 participants via
surveys (Shelton et al, 2014). While the majority of participants were also
recruited through the Regional Centers, some participants were recruited
through additional outreach, which hopefully increases representation of
individuals on the spectrum who are higher functioning and may not qualify for
Regional Center services.
Shelton and colleagues (2014) found that
children later diagnosed with ASD were 60% more likely to have been exposed to
organophosphate pesticides and 150% more likely to have been exposed to
carbamate pesticides. Like Roberts et al (2007) they determined exposure based
upon where the participants lived (Shelton et al, 2014).
The time period in which participants were
exposed to various pesticides may impact development. For example exposure to
organophosphate had a greater impact in the second and third trimester of
pregnancy, while pyrethroids had a greater impact during pre-conception and the
third trimester (Shelton et al, 2014).
The research concerning the linkage of ASD
and pesticides is still pretty limited. However, what is available has all
shown an impact if the exposure occurs during prenatal or early development.
There is still no research looking at exposure to pesticides in diet in not
only the early development, but also through the life span.
If you already have a child diagnosed with
ASD, then this research will not help you out much. Although, it may help
explain the rise in ASD rates, I think it really just opens up more questions.
Practically, if you are moving you may want
to look at any potential exposure to pesticides. It is also evidence in support
of more organic farming.
Reference
California Department of Developmental
Services. (2014). Who is eligible for services? Retrieved June 25, 2014 from http://www.dds.ca.gov/General/Eligibility.cfm
California Department of Pesticide Regulation.
(2013). Retrieved June 25, 2014 from http://www.cdpr.ca.gov/
Roberts, E. M., English, P. B., Grether, J.
K., Windham, G. C., Somberg, L., & Wolff, C. (2007). Maternal residence
near agricultural pesticide applications and autism spectrum disorders among
children in the California central valley. Environ Health Perspec, 115,
1482-1489.
Shelton, J. F., Geraghty, E. M., Tancredi,
D. J., Delwiche, L. D., Schmidt, R. J., Ritz, B., Hansen, R. L., &
Hertz-Picciotto, I. (2014). Neurodevelopmental disorders and prenatal
residential proximity to agricultural pesticides: The CHARGE study. Environ
Health Perspect; http://dx.doi.org/10.1289/ehp.1307044
Shelton, J. F., Hertz-Picciotto, I., &
Pessah, I. N. (2012). Tipping the balance of autism risk: Potential mechanisms
linking pesticides and autism. Environ Health Perspect; http://dx.doi.org/10.1289/ehp.1104553
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