Documentation that Pesticides commonly cause ADHD and Developmental Conditions in Infants and Children, Review – B. Windham (Ed.), 2010

Many studies have documented the neurological and developmental effects of pesticide exposure on infants and children(1abcde, etc.).  Among the effects are ADHD/ developmental deficits(1abcde)and birth defects/spontaneous abortions(1efh). Pyrethroid pesticides are becoming more commonly used as documentation of major effects by the organophosphate pesticides has accumulated. But pyrethroid pesticides have similar mechanisms of activity and effects as organophosphates, and studies suggest that low dose prenatal exposure to pyrethroids has the potential to produce long lasting developmental and behavioral effects through effects on the expression of xenobiotic metabolizing cytochrome P450s in brain and liver of the offspring as well as DNA damage and other neurological effects(1g).

  Likewise exposure to organochlorine compounds such as PCBs and DDEs and industrial chemicals(2abcde), as well as toxic metals such as mercury, lead, arsenic, and cadmium(3abc) have been found to cause ADHD and other neurological effects and developmental disabilities. Infants and children are more affected by toxic exposures than adults, but over 200 toxic chemicals have been documented to cause neurological effects on adults(3a).  A National Academy of Sciences study found that over 50% of births during a recent period resulted in birth defects or developmental conditions, such as ADHD, learning disabilities, mood disorders, chronic lung conditions, eczema, chronic allergies, etc. (3c).  Most of these are documented to have been caused by neonatal exposures to toxics, as per the documentation in this review.

The urine of 1,139 children between the ages of 8 and 15 were tested for six pesticide metabolites, with 119 of the children diagnosed with ADHD(1a). Children with a ten-fold increase in metabolites from the pesticide malathion (found in head lice treatments) were 55 percent more likely to be diagnosed with ADHD. Children with higher urinary dialkyl phosphate concentrations, especially dimethyl alkylphosphate (DMAP) concentrations, were more likely to be diagnosed as having ADHD. A 10-fold increase in DMAP concentration was associated with an odds ratio of 1.55 (95% confidence interval: 1.14–2.10), with adjustment for gender, age, race/ethnicity, poverty/income ratio, fasting duration, and urinary creatinine concentration. For the most-commonly detected DMAP metabolite, dimethyl thiophosphate, children with levels higher than the median of detectable concentrations had twice the odds of ADHD (adjusted odds ratio: 1.93 ) compared with children with undetectable levels. Such pesticides are commonly used in the growing of vegetables and fruit, such as strawberries.

The insecticide chlorpyrifos has been one of the most commonly used pesticides in homes. As part of an ongoing prospective cohort study in an inner-city minority population, neurotoxicant effects of prenatal exposure to chlorpyrifos were evaluated in 254 children through the first 3 years of life(1b). Highly exposed children scored, on average, 6.5 points lower on the Bayley Psychomotor Development Index and 3.3 points lower on the Bayley Mental Development Index at 3 years of age compared with those with lower levels of exposure. Children exposed to higher, compared with lower, chlorpyrifos levels were also significantly more likely to experience Psychomotor Development Index and Mental Development Index delays, attention problems, attention-deficit/hyperactivity disorder problems, and pervasive developmental disorder problems at 3 years of age.  The adjusted mean 36-month Psychomotor Development Index and Mental Development Index scores of the highly and lower exposed groups differed by only 7.1 and 3.0 points, respectively, but the proportion of delayed children in the high-exposure group, compared with the low-exposure group, was 5 times greater for the Psychomotor Development Index and 2.4 times greater for the Mental Development Index, increasing the number of children possibly needing early intervention services. Corn, wheat, and soy are the foods highest in the pesticide studied in that particular study. Encouragingly, a study out of Emory University found that when children with the high levels of pesticides were put on an organic diet, the blood pesticide levels became undetectable until conventional foods were reintroduced. Also, a study out of the University of Washington polled and studied parents who left a food co-op or retail grocer in the Seattle area, and classified children into a 75% conventional food group, or a 75% organic food group.  Urine samples were collected to look at pesticide exposure.  Switching to an organic diet lowered pesticide exposure.

A study of preschool children in Mexico found the group exposed to pesticides to have significant behavioral effects including increased aggression and violence(1e), compared to the control group exposed to lower levels of pesticides.  Students in an area with high pesticide exposure had significant deficits of energy and hand/eye coordination, as well as developmental learning deficits, balance problems, and poorer general health, compared to an area with lower pesticide exposure.        The Yaqui mothers from the area with higher pesticide exposure also reported more problems getting pregnant and higher rates of miscarriage, stillbirth, neonatal death and premature birth(1e).

A California study found a significant positive correlation between children with autism and home use of Pyrethroid insecticides by pregnant women(4).

References:

1.(a) Attention-Deficit/Hyperactivity Disorder and Urinary Metabolites of Organophosphate Pesticides, M.F. Bouchard, D.C. Bellinger,et al; PEDIATRICS, May 2010; & (b) Impact of Prenatal Chlorpyrifos Exposure on Neurodevelopment in the First 3 Years of Life Among Inner-City Children, V.A. Rauh, R. Garfinkel, et al, PEDIATRICS Vol. 118 No. 6 December 2006, pp. e1845-e1859; & (c ) Motor inhibition and learning impairments in school-aged children following exposure to organophosphate pesticides in infancy. Kofman O, Berger A, et al;  Pediatr Res. 2006 Jul;60(1):88-92; & (d) A summary of recent findings on birth outcomes and developmental effects of prenatal ETS, PAH, and pesticide exposures.  Perara FP, Rauh V, Kinney PL, et al, Neurotoxicology. 2005 Aug;26(4):573-87; & (e) Guillette E et al, “An anthropological approach to the evaluation of preschool children exposued to pesticides in Mexico”, Environmental Health perspectives, 106(6): 347-353; & (f) Reproductive outcomes in the women of the Red River Valley of the north. I. The spouses of pesticide applicators: pregnancy loss, age at menarche, and exposures to pesticides.  Garry VF, Long L, et al; J Toxicol Environ Health A. 2002 Jun 14;65(11):769-86; & Effects of Icon, a pyrethroid insecticide on early pregnancy of rats. Ratnasooriya WD, Ratnayake SS, Jayatunga YN. Hum Exp Toxicol. 2003 Oct;22(10):523-33;

   (g)Long lasting effects of prenatal exposure to deltamethrin on cerebral and hepatic cytochrome P450s and behavioral activity in rat offspring.  Johri A, Parmar D, et al; Eur J Pharmacol. 2006 Aug 21;544(1-3):58-68, & Cypermethrin-induced DNA damage in organs and tissues of the mouse: evidence from the comet assay.  Patel S, Pandey AK, et al,  Mutat Res. 2006 Sep 5;607(2):176-83; &   Effects of Pyrethroid Insecticides, B. Windham (Ed), www.flcv.com/PyrethrR.html; & (h) Neurological and Developmental Effects of Pesticides, Review, B. Windham (Ed), www.flcv.com/pesticid.html

2.(a)Prenatal organochlorine exposure and behaviors associated with attention deficit hyperactivity disorder in school-aged children.  Sagiv SK, Thurston SW, et al, Am J Epidemiol. 2010 Mar 1;171(5):593-601; &  (b)[Developmental neurotoxicity of industrial chemicals],[Article in French], Labie D, Med Sci (Paris). 2007 Oct;23(10):868-72; &(c) Exposure to hexachlorobenzene during pregnancy and children's social behavior at 4 years of age.  Ribas-Fito N, Sunver J, et al; Environ Health Perspect. 2007 Mar;115(3):447-50; & (d) Toxic threats to neurologic development of children.  Schettler T, Environ Health Perspect. 2001 Dec;109 Suppl 6:813-6; & (e)Epidemiologic evidence of relationships between reproductive and child health outcomes and environmental chemical contaminants.  Wigle DT, Arbuckle TE, et al,  J Toxicol Environ Health B Crit Rev. 2008 May;11(5-6):373-517.

3. (a)Developmental neurotoxicity of industrial chemicals. Grandjean P, Landrigan PJ. Lancet. 2006 Dec 16;368(9553):2167-78; &(b) Epidemiologic evidence of relationships between reproductive and child health outcomes and environmental chemical contaminants.  Wigle DT, Arbuckle TE, et al,  J Toxicol Environ Health B Crit Rev. 2008 May;11(5-6):373-517; &                    (c)Developmental Disabilities and Behavioral Effects of Toxic Metal Exposure, Review, B. Windham (Ed), www.flcv.com/tmlbn.html  & www.flcv.com/kidshg.html (over 300 peer-reviewed studies reviewed)

4. Introduction to Environmental influence on Psychiatric Disorders in Children and Adolescents, Hertz-Picciotto, I; Epidemiology: November 2008 - Volume 19 - Issue 6 - p S40, http://journals.lww.com/epidem/Fulltext/2008/11001/Introduction_to_Environmental_influence_on.106.aspx