3.6 Neurodevelopment After Prenatal and/or Childhood
Exposure
Many of the epidemiological studies recently published pertain to children
neurodevelopment after in utero or postnatal pyrethroid exposure (Table 6). All
studies related to prenatal exposures were longitudinal birth cohort studies, while a
cross-sectional design was used in all studies related to postnatal exposures. Cognitive, behavioral, and motor functions were examined in children and adolescents by
using questionnaires filled by parents or health professionals and/or by individual or
batteries of standardized and generally well-validated tests (e.g., Bayley Scales of
Infant Development, Wechsler Intelligence Scale for Children). Most studies found
evidence of an association between adverse neurodevelopmental outcomes in children (e.g., various early behavioral problems) and maternal urinary pyrethroid
metabolites during pregnancy (i.e., 3-PBA, cis- and/or trans-DCCA). Age- and
sex-specific associations were reported [53, 60]. However, there was no clear pattern
of effects. This may be due to differences in the study designs, for example, in the
exposure period (i.e., trimester of pregnancy) and the control of potential
confounding variables (e.g., current child exposure to pyrethroids and other environmental agents such as neurodevelopmental toxic pesticides), as well as in the
timing (3 months to 7 years of age), endpoints, and techniques/practices of child
assessment. In addition, there was substantial variability in the urinary levels of the
pyrethroid metabolites across studies (e.g., median 3-PBA level of 0.39 μg/L in [57]
vs less than the limit of detection of 0.008 μg/L in [58]). On the other hand, the few
studies available showed no consistent relationship between neurodevelopment and
pyrethroid exposure during childhood, as assessed by metabolite measurements in
the child urine.
Contrasting results have been reported regarding the association between childhood urinary 3-PBA and attention-deficit/hyperactivity disorder (ADHD) in subsets
of the US NHANES cohort (National Health and Nutrition Survey) (Table 6).
Methodological heterogeneity may have accounted for these differences (e.g., primary outcome definition, use of continuous 3-PBA levels vs dichotomized categorization detected/non-detected).
A couple of studies have focused on autism spectrum disorders (ASDs) and
developmental delays, including two retrospective case-control studies from the
Childhood Autism Risks from Genetics and Environment (CHARGE) [70, 73]
(Table 6). They have established a link between ASDs risk and residential proximity
to pyrethroid application, especially during the preconception and gestational
periods. This suggested that exposure to these pesticides during critical periods of
development may be a contributing factor to the likelihood of developing ASDs
[74, 75].
Human Risk Associated with Long-Term Exposure to Pyrethroid Insecticides
283
Exposure
Many of the epidemiological studies recently published pertain to children
neurodevelopment after in utero or postnatal pyrethroid exposure (Table 6). All
studies related to prenatal exposures were longitudinal birth cohort studies, while a
cross-sectional design was used in all studies related to postnatal exposures. Cognitive, behavioral, and motor functions were examined in children and adolescents by
using questionnaires filled by parents or health professionals and/or by individual or
batteries of standardized and generally well-validated tests (e.g., Bayley Scales of
Infant Development, Wechsler Intelligence Scale for Children). Most studies found
evidence of an association between adverse neurodevelopmental outcomes in children (e.g., various early behavioral problems) and maternal urinary pyrethroid
metabolites during pregnancy (i.e., 3-PBA, cis- and/or trans-DCCA). Age- and
sex-specific associations were reported [53, 60]. However, there was no clear pattern
of effects. This may be due to differences in the study designs, for example, in the
exposure period (i.e., trimester of pregnancy) and the control of potential
confounding variables (e.g., current child exposure to pyrethroids and other environmental agents such as neurodevelopmental toxic pesticides), as well as in the
timing (3 months to 7 years of age), endpoints, and techniques/practices of child
assessment. In addition, there was substantial variability in the urinary levels of the
pyrethroid metabolites across studies (e.g., median 3-PBA level of 0.39 μg/L in [57]
vs less than the limit of detection of 0.008 μg/L in [58]). On the other hand, the few
studies available showed no consistent relationship between neurodevelopment and
pyrethroid exposure during childhood, as assessed by metabolite measurements in
the child urine.
Contrasting results have been reported regarding the association between childhood urinary 3-PBA and attention-deficit/hyperactivity disorder (ADHD) in subsets
of the US NHANES cohort (National Health and Nutrition Survey) (Table 6).
Methodological heterogeneity may have accounted for these differences (e.g., primary outcome definition, use of continuous 3-PBA levels vs dichotomized categorization detected/non-detected).
A couple of studies have focused on autism spectrum disorders (ASDs) and
developmental delays, including two retrospective case-control studies from the
Childhood Autism Risks from Genetics and Environment (CHARGE) [70, 73]
(Table 6). They have established a link between ASDs risk and residential proximity
to pyrethroid application, especially during the preconception and gestational
periods. This suggested that exposure to these pesticides during critical periods of
development may be a contributing factor to the likelihood of developing ASDs
[74, 75].
Human Risk Associated with Long-Term Exposure to Pyrethroid Insecticides
283