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Janie F. Shelton, PhD, MPH
PRENATAL EXPOSURE
TO PESTICIDES AND
CHILD HEALTH
OUTCOMES
Quick note on definitions and scope of talk
• The term pesticides refers to a broad range of compounds including
both herbicides and insecticides.
• Of most concern for children’s health today are commonly used
insecticides, which act as neurotoxins.
• For this reason, my talk will focus on common neurotoxic
insecticides in these chemical categories:
• Organophosphates
• Pyrethroids
• Carbamates
• Organochlorines
How can insecticides influence brain
development?
• From early pregnancy, neurons are rapidly developing and
differentiating to grow and move to the correct part of the embryo
for development.
• During development, the fetus does not possess the enzymatic,
metabolic, or immunological responses that adults do, making them
more vulnerable. Further, they take in higher levels of insecticides
per Kg body weight than adults.
Organophosphates (e.g. chlorpyrifos, diazinon,
malathion, etc.)
• Organophosphates irreversibly inactivate acetylcholinesterase,
which is needed in early brain development and naturally functions
to stop neuronal cell signaling.
• Widely used in agriculture, but declining in use over time.
Pyrethroids (e.g. permethrin, bifenthrin,
esfenvalerate, etc.)
• Pyrethroids block a channel (voltage-gated sodium channel) which
also inhibits the normal shut down of neuronal cell signaling
• Commonly used in homes as flea and tick shampoo, as well as in
agriculture as a replacement to the phase-out of
organophosphates.
Childhood Autism Risks from Genetics and
Environment (CHARGE) Study
• Case-control study in Northern California
• MIND Institute, UC Davis
• Designed to evaluate environmental and genetic causes of autism
spectrum disorders (ASD) and developmental delay
• Children aged 2-5
• Cases are selected from a random sample drawn from California
Department of Developmental Services Registries
• Controls of same gender and age randomly selected from the population
and frequency matched on age, gender, and region
Epidemiology of autism spectrum disorders
(ASD)
• Developmental disorder characterized by deficits in social
interaction, restricted interests or behaviors, and deficits in
language presenting prior to age 3.
• Unknown etiology
• Epidemic rise in the United States, now affecting 1 out of 68
children (CDC, 2014), up from 1 out of 150 in 2000
• Diagnosed more often in boys than girls (5:1)
• Changing diagnosis explains some proportion of increase, but not
all.
• Primary causal theory:
• Gene X Environment interaction
• For example, genetic vulnerability + exposure to pesticides
CDC Autism Prevalence Estimates
6.7 6.6
8.0
9.0
11.3
14.7
1992 1994 1996 1998 2000 2002
0.0
2.0
4.0
6.0
8.0
10.0
12.0
14.0
16.0
Birth year
U.S. prevalence per 1,000 children
Why look at the relationship between autism
and pesticides?
• Roberts et al. (2007) found increased risk of ASD among children
born to mothers living in close proximity to organochlorine and
other pesticides applied in the California Central Valley
• Eskenazi et al. (2007) reported mothers with elevated levels of
organophosphate metabolites in the 2nd and 3rd trimesters
corresponded with an increased frequency of reporting ASD-type
symptomology in children (by parents)
• Bouchard et al. (2010) reported children with ADHD had higher
levels of organophosphate metabolites in their urine than kids
without ADHD
CHARGE Study Methods: Exposure estimation
• We utilized the California
Pesticide Use Report (PUR)
data to map agricultural
applications of neurotoxic
pesticides to the mothers
residence during pregnancy
within 1.25km, 1.5km, and
1.75km
• The PUR is a mandatory
reporting system in
California including
information on the
compound, time, date, and
location of application
Elevated risk of ASD associated with living nearby pesticide
applications during pregnancy
(adjusted odds ratios and 95% confidence intervals)
Pesticide, Buffer
radius (Km) Pregnancy
Pre-
conception 1st trimester 2nd trimester 3rd trimester
Organophosphates
1.25 1.60 (1.02, 2.51) 1.37 (0.76, 2.50) 1.53 (0.87, 2.68) 1.57 (0.87, 2.83) 1.99 (1.11, 3.56)
1.5 1.54 (1.00, 2.38) 1.38 (0.82, 2.31) 1.45 (0.88, 2.41) 1.85 (1.08, 3.15) 2.07 (1.23, 3.50)
1.75 1.26 (0.83, 1.92) 1.30 (0.80, 2.13) 1.02 (0.63, 1.65) 1.54 (0.93, 2.55) 1.99 (1.20, 3.30)
Chlorpyrifos
1.25 1.57 (0.82, 3.00) 1.07 (0.40, 2.89) 1.26 (0.52, 3.06) 2.55 (0.95, 6.84) 1.83 (0.72, 4.65)
1.5 1.66 (0.94, 2.93) 1.07 (0.46, 2.48) 1.32 (0.65, 2.70) 3.31 (1.48, 7.42) 1.78 (0.82, 3.87)
1.75 1.78 (1.05, 3.02) 1.25 (0.59, 2.65) 1.12 (0.58, 2.16) 2.63 (1.28, 5.41) 2.15 (1.04, 4.41)
Pyrethroids
1.25 1.34 (0.82, 2.20) 1.82 (0.92, 3.60) 1.59 (0.86, 2.96) 1.56 (0.83, 2.94) 1.64 (0.84, 3.19)
1.5 1.41 (0.89, 2.25) 1.82 (1.00, 3.31) 1.53 (0.88, 2.67) 1.69 (0.93, 3.06) 1.87 (1.02, 3.43)
1.75 1.27 (0.83, 1.96) 1.69 (0.97, 2.95) 1.14 (0.67, 1.91) 1.49 (0.87, 2.58) 1.83 (1.04, 3.23)
Type 2
1.25 1.40 (0.83, 2.34) 2.01 (0.97,4.16) 1.64 (0.85, 3.17) 1.29 (0.65,2.56) 1.51 (0.75, 3.05)
1.5 1.53 (0.94, 2.51) 1.98 (1.06, 3.71) 1.85 (1.01, 3.38) 1.45 (0.78, 2.73) 1.67 (0.87, 3.21)
1.75 1.30 (0.82, 2.05) 1.64 (0.92, 2.94) 1.32 (0.76, 2.29) 1.33 (0.75, 2.38) 1.56 (0.86, 2.84)
What did we learn from our research?
• Our findings support previous research indicating agricultural
pesticides may increase the risk of ASD.
• In our study, after controlling for factors such as parental education
level, race/ethnicity, year of birth, and maternal prenatal vitamin
intake, we conclude:
• Residential proximity (~1 mile) to applications of organophosphates and
pyrethroids may increase the risk of autism spectrum disorders.
• The findings for developmental delay were less conclusive.
What else do we know about the impacts of
pesticide exposure and child health?
• Prenatal exposure to chlorpyrifos is associated with lower working
memory performance and IQ scores at age 7 (Rauh V., 2011) and
brain structure anomalies (Rauh V., 2012).
• Prenatal exposure to piperonyl butoxide, a pyrethroid synergist, is
associated with diminished scores on the Mental Development
Index at 36 months (Horton M.K., 2011).
• Early life exposure to organophosphates associated with symptoms
of asthma at ages 5-7 (Raanan R., 2014)
• 31 per cent of acute pesticide illness cases in schools is associated
with drift from nearby farmland (Alarcon W.A., 2005).
What are we not sure about?
• There are likely complex relationships underlying genetic
vulnerability and pesticide exposure.
• Many avenues of exposure for expectant mothers and children
(dietary, inhalation of compound, inhalation of compound bound to
dust particles, dermal exposure from flea/tick shampoo, etc.)
• No real idea of what dose is considered safe for developing fetus
• Scientific research constrained by difficulties estimating exposure
during all windows of development and isolating effects to one
“window of vulnerability”
• Spatial models utilized thus far do not incorporate weather and wind-
direction
• Biological samples have high daily variation
Conclusions
• The State should know when and where these compounds are
applied for the purposes of monitoring and evaluation, as in the
State of California (see Pesticide Use Report, CDPR).
• Because of our research and other studies showing similar findings,
it is advised that pregnant women and children minimize exposure
to pesticides by:
• Ensuring adequate buffer zones around homes and schools
• Establish a warning or notification system if pesticides are applied very
close of the school or home
• Low or no residential use, and especially not handled by the mother during
pregnancy (e.g. flea collars for dogs, etc.)
• Consumption of organic produce whenever possible
Please contact me at
janie.shelton@gmail.com for any
further questions
MAHALO
THANK YOU

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Prenatal Exposure to Pesticides and Child Health Outcomes

  • 1. Janie F. Shelton, PhD, MPH PRENATAL EXPOSURE TO PESTICIDES AND CHILD HEALTH OUTCOMES
  • 2. Quick note on definitions and scope of talk • The term pesticides refers to a broad range of compounds including both herbicides and insecticides. • Of most concern for children’s health today are commonly used insecticides, which act as neurotoxins. • For this reason, my talk will focus on common neurotoxic insecticides in these chemical categories: • Organophosphates • Pyrethroids • Carbamates • Organochlorines
  • 3. How can insecticides influence brain development? • From early pregnancy, neurons are rapidly developing and differentiating to grow and move to the correct part of the embryo for development. • During development, the fetus does not possess the enzymatic, metabolic, or immunological responses that adults do, making them more vulnerable. Further, they take in higher levels of insecticides per Kg body weight than adults.
  • 4. Organophosphates (e.g. chlorpyrifos, diazinon, malathion, etc.) • Organophosphates irreversibly inactivate acetylcholinesterase, which is needed in early brain development and naturally functions to stop neuronal cell signaling. • Widely used in agriculture, but declining in use over time.
  • 5. Pyrethroids (e.g. permethrin, bifenthrin, esfenvalerate, etc.) • Pyrethroids block a channel (voltage-gated sodium channel) which also inhibits the normal shut down of neuronal cell signaling • Commonly used in homes as flea and tick shampoo, as well as in agriculture as a replacement to the phase-out of organophosphates.
  • 6. Childhood Autism Risks from Genetics and Environment (CHARGE) Study • Case-control study in Northern California • MIND Institute, UC Davis • Designed to evaluate environmental and genetic causes of autism spectrum disorders (ASD) and developmental delay • Children aged 2-5 • Cases are selected from a random sample drawn from California Department of Developmental Services Registries • Controls of same gender and age randomly selected from the population and frequency matched on age, gender, and region
  • 7. Epidemiology of autism spectrum disorders (ASD) • Developmental disorder characterized by deficits in social interaction, restricted interests or behaviors, and deficits in language presenting prior to age 3. • Unknown etiology • Epidemic rise in the United States, now affecting 1 out of 68 children (CDC, 2014), up from 1 out of 150 in 2000 • Diagnosed more often in boys than girls (5:1) • Changing diagnosis explains some proportion of increase, but not all. • Primary causal theory: • Gene X Environment interaction • For example, genetic vulnerability + exposure to pesticides
  • 8. CDC Autism Prevalence Estimates 6.7 6.6 8.0 9.0 11.3 14.7 1992 1994 1996 1998 2000 2002 0.0 2.0 4.0 6.0 8.0 10.0 12.0 14.0 16.0 Birth year U.S. prevalence per 1,000 children
  • 9. Why look at the relationship between autism and pesticides? • Roberts et al. (2007) found increased risk of ASD among children born to mothers living in close proximity to organochlorine and other pesticides applied in the California Central Valley • Eskenazi et al. (2007) reported mothers with elevated levels of organophosphate metabolites in the 2nd and 3rd trimesters corresponded with an increased frequency of reporting ASD-type symptomology in children (by parents) • Bouchard et al. (2010) reported children with ADHD had higher levels of organophosphate metabolites in their urine than kids without ADHD
  • 10. CHARGE Study Methods: Exposure estimation • We utilized the California Pesticide Use Report (PUR) data to map agricultural applications of neurotoxic pesticides to the mothers residence during pregnancy within 1.25km, 1.5km, and 1.75km • The PUR is a mandatory reporting system in California including information on the compound, time, date, and location of application
  • 11. Elevated risk of ASD associated with living nearby pesticide applications during pregnancy (adjusted odds ratios and 95% confidence intervals) Pesticide, Buffer radius (Km) Pregnancy Pre- conception 1st trimester 2nd trimester 3rd trimester Organophosphates 1.25 1.60 (1.02, 2.51) 1.37 (0.76, 2.50) 1.53 (0.87, 2.68) 1.57 (0.87, 2.83) 1.99 (1.11, 3.56) 1.5 1.54 (1.00, 2.38) 1.38 (0.82, 2.31) 1.45 (0.88, 2.41) 1.85 (1.08, 3.15) 2.07 (1.23, 3.50) 1.75 1.26 (0.83, 1.92) 1.30 (0.80, 2.13) 1.02 (0.63, 1.65) 1.54 (0.93, 2.55) 1.99 (1.20, 3.30) Chlorpyrifos 1.25 1.57 (0.82, 3.00) 1.07 (0.40, 2.89) 1.26 (0.52, 3.06) 2.55 (0.95, 6.84) 1.83 (0.72, 4.65) 1.5 1.66 (0.94, 2.93) 1.07 (0.46, 2.48) 1.32 (0.65, 2.70) 3.31 (1.48, 7.42) 1.78 (0.82, 3.87) 1.75 1.78 (1.05, 3.02) 1.25 (0.59, 2.65) 1.12 (0.58, 2.16) 2.63 (1.28, 5.41) 2.15 (1.04, 4.41) Pyrethroids 1.25 1.34 (0.82, 2.20) 1.82 (0.92, 3.60) 1.59 (0.86, 2.96) 1.56 (0.83, 2.94) 1.64 (0.84, 3.19) 1.5 1.41 (0.89, 2.25) 1.82 (1.00, 3.31) 1.53 (0.88, 2.67) 1.69 (0.93, 3.06) 1.87 (1.02, 3.43) 1.75 1.27 (0.83, 1.96) 1.69 (0.97, 2.95) 1.14 (0.67, 1.91) 1.49 (0.87, 2.58) 1.83 (1.04, 3.23) Type 2 1.25 1.40 (0.83, 2.34) 2.01 (0.97,4.16) 1.64 (0.85, 3.17) 1.29 (0.65,2.56) 1.51 (0.75, 3.05) 1.5 1.53 (0.94, 2.51) 1.98 (1.06, 3.71) 1.85 (1.01, 3.38) 1.45 (0.78, 2.73) 1.67 (0.87, 3.21) 1.75 1.30 (0.82, 2.05) 1.64 (0.92, 2.94) 1.32 (0.76, 2.29) 1.33 (0.75, 2.38) 1.56 (0.86, 2.84)
  • 12. What did we learn from our research? • Our findings support previous research indicating agricultural pesticides may increase the risk of ASD. • In our study, after controlling for factors such as parental education level, race/ethnicity, year of birth, and maternal prenatal vitamin intake, we conclude: • Residential proximity (~1 mile) to applications of organophosphates and pyrethroids may increase the risk of autism spectrum disorders. • The findings for developmental delay were less conclusive.
  • 13. What else do we know about the impacts of pesticide exposure and child health? • Prenatal exposure to chlorpyrifos is associated with lower working memory performance and IQ scores at age 7 (Rauh V., 2011) and brain structure anomalies (Rauh V., 2012). • Prenatal exposure to piperonyl butoxide, a pyrethroid synergist, is associated with diminished scores on the Mental Development Index at 36 months (Horton M.K., 2011). • Early life exposure to organophosphates associated with symptoms of asthma at ages 5-7 (Raanan R., 2014) • 31 per cent of acute pesticide illness cases in schools is associated with drift from nearby farmland (Alarcon W.A., 2005).
  • 14. What are we not sure about? • There are likely complex relationships underlying genetic vulnerability and pesticide exposure. • Many avenues of exposure for expectant mothers and children (dietary, inhalation of compound, inhalation of compound bound to dust particles, dermal exposure from flea/tick shampoo, etc.) • No real idea of what dose is considered safe for developing fetus • Scientific research constrained by difficulties estimating exposure during all windows of development and isolating effects to one “window of vulnerability” • Spatial models utilized thus far do not incorporate weather and wind- direction • Biological samples have high daily variation
  • 15. Conclusions • The State should know when and where these compounds are applied for the purposes of monitoring and evaluation, as in the State of California (see Pesticide Use Report, CDPR). • Because of our research and other studies showing similar findings, it is advised that pregnant women and children minimize exposure to pesticides by: • Ensuring adequate buffer zones around homes and schools • Establish a warning or notification system if pesticides are applied very close of the school or home • Low or no residential use, and especially not handled by the mother during pregnancy (e.g. flea collars for dogs, etc.) • Consumption of organic produce whenever possible
  • 16. Please contact me at janie.shelton@gmail.com for any further questions MAHALO THANK YOU