The goal was to examine the association between urinary concentrations of dialkyl phosphate metabolites of organophosphates and attention-deficit/hyperactivity disorder (ADHD) in children 8 to 15 years of age.
Cross-sectional data from the National Health and Nutrition Examination Survey (2000–2004) were available for 1139 children, who were representative of the general US population. A structured interview with a parent was used to ascertain ADHD diagnostic status, on the basis of slightly modified criteria from the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition.
One hundred nineteen children met the diagnostic criteria for 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 [95% confidence interval: 1.23–3.02]), compared with children with undetectable levels.
These findings support the hypothesis that organophosphate exposure, at levels common among US children, may contribute to ADHD prevalence. Prospective studies are needed to establish whether this association is causal.
environmental toxins and autism
The study by Bouchard et al ties organophosphate pesticide exposure to attention-deficit disorder in children. I'd like to suggest that the increasing exposure to toxic substances in the environment - including BPA in plastic baby bottles - might be responsible for the apparent rise in the incidence of autism. A great deal of evidence is now available on childhood vaccines and autism, and essentially none of it implicates vaccines as causative, or even associated. Yet, the mere suggestion that the increasing number of antigens given to infants and children seems to parallel the (apparent) increase in autism rates, amplified by the sensationalist media, has unquestionably led to falling immunization rates and the resurgence of preventable infectious diseases, some of it fatal. Might it be possible to redirect the public's attention to a much more likely culprit? Much of the general public clings to the notion that vaccines are to blame for autism, based on nothing at all except the desire to find a culprit which the individual can control. If there is an identifiable culprit, it might well be environmental toxins. Perhaps it might be possible to shift the attention of the public away from lifesaving vaccines and towards environmental contamination? More research is urgently needed, and while we await the data, perhaps public discussion of this hypothesis might take some of the pressure off child health clinicians attempting to convince skeptical parents of the safety of immunization.
Conflict of Interest:
What are your recommendations for washing fruits and vegetables? Thank you
Conflict of Interest:
Comment on Bouchard et al.: Attention-Deficit/Hyperactivity Disorder and Urinary Metabolites of Orga
In their study of the relationship of Attention-Deficit Hyperactivity Disorder (ADHD) and urinary metabolites of organophosphate pesticides in children 8-15 years old, Bouchard et al. are meticulous in their laboratory and statistical analyses, but less so in considering risk factors associated with ADHD.
Based on information from more than 20 studies, ADHD heritability has been estimated to be about 75%1. Among children with ADHD or earlier definitions of the disorder, reported proportions of at least one affected parent or sibling range from 9 % to 64%2-9. A recent rigorous analysis found that 16% to 20% of parents of children with ADHD and comorbidities also had ADHD10.
Bouchard et al. report a significant increase in the risk of the hyperactive/compulsive subtype of ADHD with a 10-fold increase in urinary dimethyl alkyl phosphate (DMAP) concentration. It is likely that inclusion of family history of psychopathology in the researchers’ statistical modeling would have reduced the strength of this association or eliminated it entirely. Since the authors obviously went to considerable effort to interview mothers or other caretakers of study subjects, it is not clear why they did not obtain a family history. This is like investigating a risk factor for breast cancer without controlling for family history of the disease or lung cancer without controlling for smoking history11,12.
Hopefully, future ADHD research will give appropriate consideration to all known or suspected risk factors.
1. Biederman J, Faraone SV. Attention-deficit hyperactivity disorder. Lancet. 2005;366(9481):237-248.
2. Morrison JR, Stewart MA. 1971. A family study of the hyperactive child syndrome. Biol Psychiatry. 1971;3(3):189-195.
3. Cantwell DP. Psychiatric illness in the families of hyperactive children. Archives of General Psychiatry. 1972;27(3):414-417.
4. Biederman J, Faraone SV, Keenan K, Knee D, Tsuang MT. Family- genetic and psychosocial risk factors in DSM-III attention deficit disorder. J Am Acad Child Adolesc Psychiatry. 1990;29(4):526-533.
5. Schachar R, Wachsmuth R. Hyperactivity and parental psychopathology. J Child Psychol Psychiatry. 1990;31(3):381-392.
6. Roizen NJ, Blondis TA, Irwin M, Rubinoff A, Kieffer J, Stein MA. Psychiatric and developmental disorders in families of children with attention-deficit hyperactivity disorder. Arch Pediatr Adolesc Med. 1996;150(2):203-208.
7. Milberger S, Faraone SV, Biederman J, Chu MP, Wilens T. Familial risk analysis of the association between attention-deficit/hyperactivity disorder and psychoactive substance use disorders. Arch Pediatr Adolesc Med. 1998;152(10):945-951.
8. Biederman J. Advancing the neuroscience of ADHD: Attention- Deficit/Hyperactivity Disorder: A Selective Overview. Biol Psychiatry. 2005;57(11):1215-1220.
9. Goos LM, Ezzatian P, Shachar R. Parent-of-origin effects on attention-deficit hyperactivity disorder. Psychiatry Research. 2007;149(1- 3):1-9.
10. Biederman J, Petty CR, Wilens TE, Fraire MG, Purcell CA, Mick E, et al. Familial risk analysis of attention deficit hyperactivity disorder and substance use disorders. Am J Psychiatry. 2008;165:107-115.
11. Kelsey JL, Gammon MD. Epidemiology of breast cancer. Epidemiol Rev. 1990;12:228-240.
12. Stevens RG, Moolgavkar SH. 1979. Estimation of relative risk from vital data: smoking and cancers of the lung and bladder. Journal of the National Cancer Institute. 1979;63(6):1351-1357.
Word count: total: 495
Conflict of Interest:
ADHD and Environment
The work done here adds to the growing list of environmental risk factors for ADHD. These include but are not limited to elevated lead exposure (1), deficiency in iron (2), and deficiency in zinc (3). Of interest is that in an animal model, dietary zinc has a protective effect upon exposure to organophosphates, and organophosphate exposure leads to low levels of zinc (4). So while genetic risks for ADHD lead us to ponder, environmental risks for ADHD call us to act.
1. Nigg, Joel, et al., "Confirmation and extension of association of blood lead with ADHD and ADHD symptom domains at population-typical exposure levels", Journal of Child Psychology and Psychiatry, and Applied Disciplines, 2010 Jan; 51(1): 58-65.
2. Konofal, Eric, et al., “Iron deficiency in children with attention-deficit / hyperactivity disorder”, Archives of Pediatrics and Adolescent Medicine, 2004 Dec; 158(12): 1113-5.
3. Bilici, Mustafa, et al., "Double -blind, placebo controlled study of zinc sulfate in the treatment of attention deficit hyperactivity disorder", Progress in Neuro-Psychopharmacology & Biological Psychiatry, 2004 June; 28(1): 181-90.
4. Goel, Ajay and Dhawan, Devinder, "Zinc Supplementation Prevents Liver Injury in Chlorpyrifos-Treated Rats", Biological Trace Element Research, 2001 June; 82(1-3): 185-200.
Conflict of Interest: