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Pesticide-Induced Diseases: Learning/Developmental Disorders

Attention Deficit Hyperactivity Disorder ● Autism ● Developmental Delays

Roughly one in six children in the U.S. has one or more developmental disabilities, ranging from a learning disability to a serious behavioral or emotional disorder. Scientists believe that the amount of toxic chemicals in the environment that cause developmental and neurological damage are contributing to the rise of physical and mental effects being found in children. Studies show children’s developing organs create “early windows of great vulnerability” during which exposure to pesticides can cause great damage. In the U.S., requirements for testing pesticides and other chemicals for potential developmental and learning disorders are minimal.

A developing brain is much more susceptible to the toxic effects of chemicals than an adult brain. During development, the brain undergoes a highly complex series of processes at different stages. Interference from toxic substances that disrupt these processes can have permanent consequences. That vulnerability extends from fetal development through infancy and childhood to adolescence. Research has shown that environmental toxicants, such as pesticides, at low levels of exposure can have subclinical effects—not clinically visible, but still important adverse effects, such as decreases in intelligence or changes in behavior.

Attention Deficit Hyperactivity Disorder (ADHD)

Autism

  • Tipping the Balance of Autism Risk: Potential Mechanisms Linking Pesticides and Autism
    Autism spectrum disorders (ASDs) have been increasing in many parts of the world and a portion of cases are attributable to environmental exposures. Conclusive replicated findings have yet to appear on any specific exposure; however, mounting evidence suggests gestational pesticides exposures are strong candidates.Authors review and discuss previous research related to autism risk, developmental effects of early pesticide exposure, and basic biological mechanisms by which pesticides may induce or exacerbate pathophysiological features of autism. In experimental and observational research, certain pesticides may be capable of inducing core features of autism, but little is known about the timing or dose, or which of various mechanisms is sufficient to induce this condition. In animal studies, authors encourage more research on gene × environment interactions, as well as experimental exposure to mixtures of compounds. Similarly, epidemiologic studies in humans with exceptionally high exposures can identify which pesticide classes are of greatest concern, and studies focused on gene × environment are needed to determine if there are susceptible subpopulations at greater risk from pesticide exposures.
    [Shelton, J.F., Hertz-Picciotto, I. and Pessah, I.H. 2012. Environ Health Persp. 120 (7): 944-951.]
  • A macroepigenetic approach to identify factors responsible for the autism epidemic in the United States
    The demand for special education services continues to rise in disability categories associated with pervasive developmental disorders. Neurodevelopment can be adversely impacted when gene expression is altered by dietary transcription factors, such as zinc insufficiency or deficiency, or by exposure to toxic substances found in our environment, such as mercury or organophosphate pesticides. Gene expression patterns differ geographically between populations and within populations. Gene variants of paraoxonase-1 are associated with autism in North America, but not in Italy, indicating regional specificity in gene-environment interactions. In the current review, authors utilize a novel macroepigenetic approach to compare variations in diet and toxic substance exposure between these two geographical populations to determine the likely factors responsible for the autism epidemic in the United States.
    [Dufault, R., W.J. Lukiw, R. Crider, R. Schnoll, D. Wallinga and R. Deth. 2012. Clinical Epigenetics. 4(1):6]
  • A Research Strategy to Discover the Environmental Causes of Autism and Neurodevelopmental Disabilities
    This editorial explores the ongoing research, both genetic and environmental studies,to identify the potentially preventable causes of neuro-develop-mental disorders (NDDs). Genetic research has demonstrated that austism spectrum disorder (ASD) and certain other NDDs have a strong hereditary component. Exploration of the environmental causes of autism and other NDDs has been catalyzed by growing recognition of the exquisite sensitivity of the developing human brain to toxic chemicals. This susceptibility is greatest during unique “windows of vulnerability” that open only in embryonic and fetal life and have no later counter-part. Additional prospective studies have linked loss of cognition (IQ), dyslexia, and ADHD to lead, methyl-mercury, organophosphate insecticides, organo-chlorine insecticides, polychlorinated biphenyls, arsenic and others.A major unanswered question is whether there are still undiscovered environ-mental causes of autism or other NDDs among the thousands of chemicals currently in wide use in the United States. The significance of early chemical exposures for children’s health is not yet fully understood. A great concern is that a large number of the chemicals in widest use have not undergone even minimal assessment of potential toxicity, and only about 20% have been screened for potential toxicity during early development. Unless studies specifically examine develop-mental consequences of early exposures to untested chemicals, sub-clinical dysfunction caused by these exposures can go unrecognized for years.
    [Landrigan P.J., Lambertini,L and Birnbaum, L.S. 2012. Environ Health Perspect. 120(7): a258-a260]
  • The Rise in Autism and the Role of Age at Diagnosis.
    Study found that a seven- to eight-fold increase in the number children born in California with autism since 1990. These results suggest that research should shift from genetics to the host of chemicals and infectious microbes in the environment that are likely at the root of changes in the neurodevelopment of California’s children, including pesticides and household chemicals.
    [Hertz-Picciotto, I. and Delwiche, L. 2009. Epidemiology:20(1) - pp 84-90 doi: 10.1097/EDE.0b013e3181902d15]
  • Household Pesticide Use in Relation to Autism
    A population-based study looking at how genes and environmental factors interact shows that pet shampoos containing insecticides may trigger autism spectrum disorders (ASD). The study findings, presented at the International Meeting for Autism Research, show that mothers of children with an ASD are twice as likely to have used an insecticidal pet shampoo during the prenatal and/or postnatal period when compared to mothers of healthy children. The strongest association was during the second trimester of pregnancy.
    [Hertz-Picciotto, et al. Oral Presentation at the International Meeting for Autism Research (ORAL 2899). London, England, May 15, 2008)]
  • Autism: Transient in utero hypothyroxinemia related to maternal flavonoid ingestion during pregnancy and to other environmental antithyroid agents
    Author suggests that substances that interfere with thyroidal activity may produce morphological brain changes leading to autism. Environmental contaminants interfere with thyroid function including 60% of all herbicides, in particular 2,4-D, acetochlor, aminotriazole, amitrole, bromoxynil, pendamethalin, mancozeb, and thioureas. The current surge of autism could be related to transient maternal hypothyroxinemia resulting from dietary and/or environmental exposure to antithyroid agents.
    [Román, G, C. 2007. Journal of the Neurological Sciences; 262(1-2), pp 15-26]
  • Maternal Residence Near Agricultural Pesticide Applications and Autism Spectrum Disorders Among Children in the California Central Valley.
    Study shows that children born to mothers living near agricultural fields where organochlorine pesticides, specifically endosulfan and dicofol, were applied during their first trimester of pregnancy were six times more likely to have children that develop autism spectrum disorders (ASDs). compared to mothers who did not live near the fields.
    [Roberts, E, M. et al. 2007. Environ Health Perspect 115:1482-1489. doi:10.1289/ehp.10168]

Developmental Delays

  • Does the home environment and the sex of the child modify the adverse effects of prenatal exposure to chlorpyrifos on child working memory?
    In the current paper, the authors expanded the previous work on CPF to investigate how additional biological and social environmental factors might create or explain differential neurodevelopmental susceptibility, focusing on main and moderating effects of the quality of the home environment (HOME) and child sex. The study evaluate how the quality of the home environment (specifically, parental nurturance and environmental stimulation) and child sex interact with the adverse effects of prenatal CPF exposure on working memory at child age 7years. Results found a borderline significant interaction between prenatal exposure to CPF and child sex suggesting males experience a greater decrement in working memory than females following prenatal CPF exposure. In addition, a borderline interaction between parental nurturance and child sex was detected suggesting that, in terms of working memory, males benefit more from a nurturing environment than females. This is the first investigation into factors that may inform an intervention strategy to reduce or reverse the cognitive deficits resulting from prenatal CPF exposure.
    [Horton, M.K., L.G. Kahn, F. Perera, D.B. Barr and V. Rauh. 2012. Neurotoxicology and Teratology. 34(5):534-41]
  • Brain anomalies in children exposed prenatally to a common organophosphate pesticide
    Study investigated associations between chlorpyrifos (CPF) exposure and brain morphology using magnetic resonance imaging in 40 children selected from a nonclinical, representative community-based cohort. High CPF exposure was associated with enlargement of superior temporal, posterior middle temporal, and inferior postcentral gyri bilaterally, and enlarged superior frontal gyrus, gyrus rectus, cuneus, and precuneus along the mesial wall of the right hemisphere. A significant exposure × IQ interaction was derived from CPF disruption of normal IQ associations with surface measures in low-exposure children. In preliminary analyses, high-exposure children did not show expected sex differences in the right inferior parietal lobule and superior marginal gyrus, and displayed reversal of sex differences in the right mesial superior frontal gyrus, consistent with disruption by CPF of normal behavioral sexual dimorphisms reported in animal models. High-exposure children also showed frontal and parietal cortical thinning, and an inverse dose–response relationship between CPF and cortical thickness.
    [Rauh, V. A., F. P. Perera, M. K. Horton, R. M. Whyatt, et al. 2012. PNAS.109 (20): 7871-6.]
  • Prenatal Exposure to Organophosphates, Paraoxonase 1, and Cognitive Development in Childhood
    Researchers examine the relationship between biomarkers of organophosphate exposure, PON1, and cognitive development at ages 12 and 24 months, and 6 to 9 years in this Mount Sinai Children’s Environmental Health Study. Prenatal exposurel was associated with a decrement in mental development at 12 months among blacks and Hispanics. In later childhood, increasing pesticide metabolites were associated with decrements in perceptual reasoning, with a monotonic trend consistent with greater decrements with increasing prenatal exposure. Findings suggest that prenatal exposure to organophosphates negatively impacts cognitive development, particularly perceptual reasoning, with evidence of effects beginning at 12 months and continuing through early childhood.
    [Engel SM, Wetmur J, Chen J, Zhu C, Barr DB, Canfield RL, et al. 2011. Environ Health Perspect :-. doi:10.1289/ehp.1003183]
  • 7-Year Neurodevelopmental Scores and Prenatal Exposure to Chlorpyrifos, a Common Agricultural Pesticide
    This is a longitudinal birth cohort study of inner-city mothers and children (Columbia Center for Children’s Environmental Health) to estimate the relationship between prenatal chlorpyrifos (CPF) exposure and neurodevelopment among cohort children at age 7 years. 265 children were sampled and researchers measured prenatal CPF exposure using umbilical cord blood plasma (picograms/gram plasma), and 7-year neurodevelopment. On average, for each standard deviation increase in exposure (4.61 pg/g), Full-Scale IQ declined by 1.4%, and Working Memory declined by 2.8%. These findings are important in light of continued widespread use of CPF in agricultural settings and possible longer-term educational implications of early cognitive deficits.
    [Rauh V, Arunajadai S, Horton M, Perera F, Hoepner L, Barr DB, et al. 2011. Environ Health Perspect. doi:10.1289/ehp.1003160]
  • Prenatal Exposure to Organophosphate Pesticides and IQ in 7-Year Old Children
    Study conducted a birth-cohort study (CHAMACOS) among predominantly Latino farmworker families from an agricultural community in California and assessed exposure to OP pesticides by measuring dialkyl phosphate (DAP) metabolites in urine collected during pregnancy and from children at age 6 months and 1, 2, 3½ and 5 years. Averaged maternal DAP concentrations were associated with poorer scores for Working Memory, Processing Speed, Verbal Comprehension, Perceptual Reasoning, and Full Scale IQ. Children in the highest quintile of maternal DAP concentrations had an average deficit of 7.0 IQ-points compared with those in the lowest quintile.
    [Bouchard MF, Chevrier J et al. 2011. Environ Health Perspect :-. doi:10.1289/ehp.1003185]
  • Trends in the Prevalence of Developmental Disabilities in US Children, 1997–2008
    A new report by the American Academy of Pediatrics reveals that roughly one in six children in the U.S. have developmental disabilities, particularly those that are linked to environmental exposure, which showcases the need for stricter policies to reduce the use of pesticides and other toxic chemicals. The study is based on National Health Interview Surveys of children aged 3 to 17 years over the 12-year period of 1997-2008. Results show that boys have a higher prevalence overall and for a number of select disabilities compared with girls. Prevalence of any developmental disability increased from 12.84% to 15.04% over 12 years. Autism, attention deficit hyperactivity disorder, and other developmental delays increased, whereas hearing loss showed a significant decline. These trends were found in all of the sociodemographic subgroups, except for autism in non-Hispanic black children. Daily News
    [Boyle, C. et al 2011. American Academy of Pediatrics, (doi: 10.1542/peds.2010-2989]
  • Impact of Prenatal Exposure to Piperonyl Butoxide and Permethrin on 36-Month Neurodevelopment
    Research published February 7, 2011 in the online edition of the journal Peditatrics shows that children more highly exposed to pyrethroid insecticides and piperonyl butoxide (PBO), a synergist added to increase the potency of pyrethroids, are three times as likely to have a mental delay compared to children with lower levels. The study measured exposure to pesticides using maternal and umbilical cord plasma samples and in personal air samples, collected using backpack air monitors during pregnancy. Children were then tested for cognitive and motor development (using the Bayley Scales of Infant Development) at three years of age. Children with the highest prenatal exposures scored about 4 points lower on the test. That’s about the same intelligence loss caused by lead, Philip Landrigan, MD, a pediatrics professor and environmental health expert at New York’s Mount Sinai School of Medicine, told USA Today. Pyrethroid pesticides kill bugs by “being toxic to the developing brain,” Dr. Landrigan says. The results are “very believable and should be taken seriously.”
    [Horton, et al. 2011. Pediatrics, Online February 7, 2011 (doi:10.1542/peds.2010-0133)]
  • Neurobehavioral Deficits and Increased Blood Pressure in School-Age Children Prenatally Exposed to Pesticides
    Prenatal exposure to pesticides at levels that do not cause adverse health effects in the mother can lead to delayed brain developmental in the child. A definite negative effect was found in children, whose mother had been exposed to pesticides during pregnancy. The effect was the strongest for motor coordination, spatial performance and visual memory. Children were 1.5 to 2 years behind in the development of these functions, which is a very marked shift at age 6-to-8 years, where brain development is particularly rapid. The researchers also found increased blood pressure, likely a result of adverse effect on brain nuclei responsible for regulation of cardiovascular functions.
    [Harari, R. et al. 2010. Environ Health Perspect, 118:890–896]
  • PON1 and Neurodevelopment in Children from the CHAMACOS Study Exposed to Organophosphate Pesticides in Utero
    Paraoxonase 1 (PON1) detoxifies oxon derivatives of some organophosphate (OP) pesticides, and its genetic polymorphisms influence enzyme activity and quantity.Study ained to determine whether PON1 genotypes and enzyme measurements were associated with child neurobehavioral development and whether PON1 modified the association of in utero exposure to OPs (as assessed by maternal DAPs) and neurobehavior.Children with the PON1−108T allele had poorer MDI scores and somewhat poorer PDI scores. Children were less likely to display PDD when they or their mothers had higher ARYase activity and when their mothers had higher POase activity.Study concludes PON1 was associated with child neurobehavioral development, but additional research is needed to confirm whether it modifies the relation with in utero OP exposure.
    [Eskenazi B., K. Huen, A. Marks, K.G.Harley, A. Bradman, D.B. Barr, et al. 2010. Environ Health Perspect. 118: 1775-1781]
  • Chlorpyrifos Exposure and Urban Residential Environment Characteristics as Determinants of Early Childhood Neurodevelopment
    Study found that high concentrations of chlorpyrifos in umbilical cord blood (>6.17 pg/g) corresponds to a 6.5 point decrease in the Psychomotor Development Index, and a 3.3 point decrease in the Mental development index in 3 year olds.The study examined neighborhood characteristics such as poverty levels and dilapidated housing, factors that are also linked to lower test scores. Researchers were able to conclude that neighborhood characteristics and chlorpyrifos exposure were independently associated with children’s neurodevelopment.
    [Lovasi , G. et al. 2010. Am J Public Health. AJPH.2009.168419v1]
  • Mind, Disrupted: How Toxic Chemicals May Affect How We Think and Who We Are
    First-ever biomonitoring report identifying toxic chemical pollution in people from the learning and developmental disability community. Report examines 61 toxic chemicals present in project participants in the context of rising rates of autism, attention-deficit hyperactivity disorder, and other learning and developmental disabilities.
    [Gonzalez, S. et al. 2010. The Learning and Developmental Disabilities Initiative]
  • Prenatal Airborne Polycyclic Aromatic Hydrocarbon Exposure and Child IQ at Age 5 Years.
    A mother’s exposure to urban air pollutants known as polycyclic aromatic hydrocarbons (PAHs) can adversely affect a child’s intelligence quotient or IQ. The Study found that children exposed to high levels of PAHs in New York City had full scale and verbal IQ scores that were 4.31 and 4.67 points lower than those of less exposed children.
    [Perera, F. et al. 2009. Pediatrics, DOI: 10.1542/peds.2008-3506]
  • Influence of Glutathione S-Transferase Polymorphisms on Cognitive Functioning Effects Induced by p,p’-DDT among Preschoolers
    Study used data from 326 children assessed in a prospective population-based birth cohort at the age of 4 years. In that study, the McCarthy Scales of Children's Abilities were administrated by psychologists, organochlorine compounds were measured in cord serum, and genotyping was conducted for the coding variant Ile105Val from GSTP1 and for null alleles from GSTM1 and GSTT1. This study used linear regression models to measure the association between organochlorines and neurodevelopmental scores by GST polymorphisms. p,p'-DDT cord serum concentration was inversely associated with general cognitive, memory, quantitative, and verbal skills, as well as executive function and working memory, in children who had any GSTP1 Val-105 allele. GSTP1 polymorphisms and prenatal p,p'-DDT exposure showed a statistically significant interaction for general cognitive skills, quantitative skills, executive function, and working memory. There were no significant associations between p,p'-DDT and cognitive functioning at 4 years of age according to GSTM1 and GSTT1 polymorphisms. Results indicate that children with GSTP1 Val-105 allele were at higher risk of the adverse cognitive functioning effects of prenatal p,p'-DDT exposure.
    [Morales E, Sunyer J, Castro-Giner F, Estivill X, et al. 2008. Environ Health Perspect. 116(11):1581-5.]
  • Neonatal Exposure to Low Doses of Diazinon: Long-Term Effects on Neural Cell Development and Acetylcholine Systems
    Researchers gave diazinon (DZN) to newborn rats on postnatal days 1-4, using doses (0.5 or 2 mg/kg) spanning the threshold for barely detectable cholinesterase inhibition, then evaluated the lasting effects on indices of neural cell number and size, and on functional markers of acetylcholine (ACh) synapses (choline acetyltransferase, presynaptic high-affinity choline transporter, nicotinic cholinergic receptors) in a variety of brain regions. DZN exposure produced a significant overall increase in cell-packing density in adolescence and adulthood, suggestive of neuronal loss and reactive gliosis; however, some regions (temporal/occipital cortex, striatum) showed evidence of net cell loss, reflecting a greater sensitivity to neurotoxic effects of DZN. Deficits were seen in ACh markers in cerebrocortical areas and the hippocampus, regions enriched in ACh projections. In contrast, there were no significant effects in the midbrain, the major locus for ACh cell bodies.These results indicate that developmental exposures to apparently nontoxic doses of DZN compromise neural cell development and alter ACh synaptic function in adolescence and adulthood. The patterns seen here differ substantially from those seen in earlier work with chlorpyrifos, reinforcing the concept that the various organophosphates have fundamentally different effects on the developmental trajectories of specific neurotransmitter systems, unrelated to their shared action as cholinesterase inhibitors.
    [Slotkin TA, Bodwell BE, Levin ED, Seidler FJ.2008. Environ Health Perspect. 116(3):340-8]
  • Prenatal Organochlorine Exposure and Measures of Behavior in Infancy Using the Neonatal Behavioral Assessment Scale (NBAS)
    Findings provide evidence for an association between low-level prenatal PCB and DDE exposures and poor attention in early infancy.
    [Sagiv SK, et al. 2008. Environ Health Perspect 116:666-673. doi:10.1289/ehp.10553]
  • In Utero p,p’-DDE Exposure and Infant Neurodevelopment: A Perinatal Cohort in Mexico
    The goal of this study was to assess the prenatal DDE exposure window and its effect on the psychomotor development index (PDI) and mental development index (MDI) during the first year of life. Authors recruited 244 children whose pregnancies and deliveries were uncomplicated, and whose mothers were monitored throughout the pregnancy. Participating mothers were not occupationally exposed to DDT (dichlorodiphenyltrichloroethane) but were residents of a zone in Mexico with endemic malaria. Third-trimester DDE level was significantly higher than the level at baseline, first, and second trimesters, but the differences never exceeded 20%. Only DDE levels during the first trimester of pregnancy were associated with a significant reduction in PDI. DDE was not associated with MDI.
    A critical window of exposure to DDE in utero may be the first trimester of the pregnancy, and psychomotor development is a target of this compound. Residues of DDT metabolites may present a risk of developmental delay for years after termination of DDT use.
    [Torres-Sánchez, L, Rothenberg,S, Schnaas, L, et al. 2007. Environ Health Perspect. 115(3): 435–439.]
  • Pesticide Exposure and Stunting as Independent Predictors of Neurobehavioral Deficits in Ecuadorian School Children
    Children in Ecuador whose mothers were exposed to pesticides while pregnant have diminished ability to copy geometric figures as part of a standardized Stanford-Binet test as compared to a control group, according to the epidemiological study. Adjusted regression analysis indicates that the exposed children experience a developmental delay on this aptitude of four years. The researchers also concluded that prenatal pesticide exposure may add to the already deleterious effects of malnutrition.
    [Grandjean, P. et al. 2006. Pediatrics, 117(3) pp. e546-e556]
  • Impact of Prenatal Chlorpyrifos Exposure on Neurodevelopment in the First 3 Years of Life Among Inner-City Children
    A 2006 study linked the insecticide chlorpyrifos, which is used on some fruits and vegetables, with delays in learning rates, reduced physical coordination, and behavioral problems in children.
    [Rauh, V. et al. 2006. Pediatrics, 118(6) pp. e1845-e1859 ]
  • In Utero Exposure to Dichlorodiphenyltrichloroethane (DDT) and Dichlorodiphenyldichloroethylene (DDE) and Neurodevelopment Among Young Mexican American Children
    Study investigated the relationship between prenatal exposure to dichlorodiphenyltrichloroethane (DDT) and dichlorodiphenyldichloroethylene (DDE) and neurodevelopment of Mexican farm-workers' children in California. Participants from the Center for the Health Assessment of Mothers and Children of Salinas study, a birth cohort study, included 360 singletons with maternal serum measures of p,p'-DDT, o,p'-DDT, and p,p'-DDE. Psychomotor development and mental development were assessed with the Bayley Scales of Infant Development at 6, 12, and 24 months. Results found a approximately 2-point decrease in Psychomotor Developmental Index scores with each 10-fold increase in p,p'-DDT levels at 6 and 12 months (but not 24 months) and p,p'-DDE levels at 6 months only. We found no association with mental development at 6 months but a 2- to 3-point decrease in Mental Developmental Index scores for p,p'-DDT and o,p'-DDT at 12 and 24 months, corresponding to 7- to 10-point decreases across the exposure range. Even when mothers had substantial exposure, breastfeeding was usually associated positively with Bayley scale scores. Prenatal exposure to DDT, and to a lesser extent DDE, was associated with neurodevelopmental delays during early childhood, although breastfeeding was found to be beneficial even among women with high levels of exposure. Countries considering the use of DDT should weigh its benefit in eradicating malaria against the negative associations found in this first report on DDT and human neurodevelopment.
    [Eskenazi B, Marks AR, Bradman A, Fenster L, et al. 2006. Pediatrics.118(1):233-41.]
  • Developmental neurotoxicity of industrial chemicals.
    Neurodevelopmental disorders such as autism, attention deficit disorder, mental retardation, and cerebral palsy are common, costly, and can cause lifelong disability. Their causes are mostly unknown. A few industrial chemicals (eg, lead, methylmercury, polychlorinated biphenyls [PCBs], arsenic, and toluene) are recognised causes of neurodevelopmental disorders and subclinical brain dysfunction. Exposure to these chemicals during early fetal development can cause brain injury at doses much lower than those affecting adult brain function. Recognition of these risks has led to evidence-based programmes of prevention, such as elimination of lead additives in petrol. Although these prevention campaigns are highly successful, most were initiated only after substantial delays. Another 200 chemicals are known to cause clinical neurotoxic effects in adults. Despite an absence of systematic testing, many additional chemicals have been shown to be neurotoxic in laboratory models. The toxic effects of such chemicals in the developing human brain are not known and they are not regulated to protect children. The two main impediments to prevention of neurodevelopmental deficits of chemical origin are the great gaps in testing chemicals for developmental neurotoxicity and the high level of proof required for regulation. New, precautionary approaches that recognise the unique vulnerability of the developing brain are needed for testing and control of chemicals.
    [Grandjean P and Landrigan PJ.2006. Lancet.368(9553):2167-78]
  • Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs.
    Pyrethroid insecticides have been used for more than 40 years and account for 25% of the worldwide insecticide market. Although their acute neurotoxicity to adults has been well characterized, information regarding the potential developmental neurotoxicity of this class of compounds is limited. There is a large age dependence to the acute toxicity of pyrethroids in which neonatal rats are at least an order of magnitude more sensitive than adults to two pyrethroids. There is no information on age-dependent toxicity for most pyrethroids. In the present review authors examine the scientific data related to potential for age-dependent and developmental neurotoxicity of pyrethroids. As a basis for understanding this neurotoxicity, authors discuss the heterogeneity and ontogeny of voltage-sensitive sodium channels, a primary neuronal target of pyrethroids. Authors also summarize 22 studies of the developmental neurotoxicity of pyrethroids and review the strengths and limitations of these studies. These studies examined numerous end points, with changes in motor activity and muscarinic acetylcholine receptor density the most common. Many of the developmental neurotoxicity studies suffer from inadequate study design, problematic statistical analyses, use of formulated products, and/or inadequate controls. These factors confound interpretation of results. To better understand the potential for developmental exposure to pyrethroids to cause neurotoxicity, additional, well-designed and well-executed developmental neurotoxicity studies are needed. These studies should employ state-of-the-science methods to promote a greater understanding of the mode of action of pyrethroids in the developing nervous system.
    [Shafer TJ, Meyer DA, Crofton KM.2005. Environ Health Perspect. 113(2):123-36.]
  • In Utero Pesticide Exposure, Maternal Paraoxonase Activity, and Head Circumference.
    Although the use of pesticides in inner-city homes of the United States is of considerable magnitude, little is known about the potentially adverse health effects of such exposure. Recent animal data suggest that exposure to pesticides during pregnancy and early life may impair growth and neurodevelopment in the offspring. To investigate the relationship among prenatal pesticide exposure, paraoxonase (PON1) polymorphisms and enzyme activity, and infant growth and neurodevelopment, authors conducted a prospective, multiethnic cohort study of mothers and infants delivered at Mount Sinai Hospital in New York City. In this report the effects of pesticide exposure on birth weight, length, head circumference, and gestational age among 404 births between May 1998 and May 2002 were evaluated. Pesticide exposure was assessed by a prenatal questionnaire administered to the mothers during the early third trimester as well as by analysis of maternal urinary pentachlorophenol levels and maternal metabolites of chlorpyrifos and pyrethroids. When the level of maternal PON1 activity was taken into account, maternal levels of chlorpyrifos above the limit of detection coupled with low maternal PON1 activity were associated with a significant but small reduction in head circumference. In addition, maternal PON1 levels alone, but not PON1 genetic polymorphisms, were associated with reduced head size. Because small head size has been found to be predictive of subsequent cognitive ability, these data suggest that chlorpyrifos may have a detrimental effect on fetal neurodevelopment among mothers who exhibit low PON1 activity.
    [Berkowitz GS, Wetmur JG, Birman-Deych E, Obel J, et al. 2004. Environ Health Perspect.112(3):388-91.]
  • Arrested Development: A study on the Human Health Impacts of Pesticides
    A study found a strong link between pesticide exposure and cognitive abilities among farmers' children in India. The study revealed serious mental development disorders that ranged from severely impaired analytical abilities, motor skills, concentration and memory among the children in the chemical-intensive cotton belts of India (A 2004 study reveals serious mental development disorders that range from severely impaired analytical abilities, motor skills, concentration and memory among the children in the chemical-intensive cotton belts of India.
    [Kuruganti, K. 2003. Greenpeace. Bangalore India.]
  • In Harms Way: Toxic Threats to Child Development.
    Animal studies link pesticides in the organochlorine, organophosphate (OP), and pyrethroid families to hyperactivity. OPs are also linked to developmental delays, behavioral disorders and motor dysfunction in animal studies.
    [Shettler, T., et al., 2000. Greater Boston Physicians for Social Responsibility: Cambridge, MA.]
  • Pesticides and Inner-city Children: Exposures, Risks, and Prevention.
    The organophosphate insecticide chlorpyrifos and certain pyrethroids are the registered pesticides most heavily applied in cities. Illegal street pesticides are also in use, including tres pasitos (a carbamate), tiza china, and methyl parathion. In New York State in 1997, the heaviest use of pesticides in all counties statewide was in the urban boroughs of Manhattan and Brooklyn. Compounding these risks of heavy exposures are children's decreased ability to detoxify and excrete pesticides and the rapid growth, development, and differentiation of their vital organ systems. These developmental immaturities create early windows of great vulnerability. Recent experimental data suggest, for example, that chlorpyrifos may be a developmental neurotoxicant and that exposure in utero may cause biochemical and functional aberrations in fetal neurons as well as deficits in the number of neurons. Certain pyrethroids exert hormonal activity that may alter early neurologic and reproductive development. Assays currently used for assessment of the toxicity of pesticides are insensitive and cannot accurately predict effects to children exposed in utero or in early postnatal life. Protection of American children, and particularly of inner-city children, against the developmental hazards of pesticides requires a comprehensive strategy that monitors patterns of pesticide use on a continuing basis, assesses children's actual exposures to pesticides, uses state-of-the-art developmental toxicity testing, and establishes societal targets for reduction of pesticide use.
    [Landrigan,PJ, Claudio,L, Markowitz, SB et al. 1999. Environ Health Perspect. 107(Suppl 3): 431–437.]
  • An Anthropological Approach to the Evaluation of Preschool Children Exposed to Pesticides in Mexico
    In a comparative study in Mexico, children exposed to pesticides demonstrated decreases in stamina, coordination, memory, and the ability to draw familiar subjects.
    [Guillette, E., et al. 1998. Environmental Health Perspectives, 106(6):347-353.]