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Several environmental risk factors have been associated with the potential development of attention-deficit hyperactivity disorder (ADHD) or hyperkinetic disorder (HKD).1-7

Pregnancy/early childhood risk factors

Data from the Quebec Longitudinal Study of Child Development were analysed to identify pregnancy/early childhood risk factors associated with symptoms of ADHD.3 In total, 2057 children participated: assessments took place at approximately yearly intervals from the age of 5 months until the age of 8 years.

The study reported several early risk factors for later development of ADHD symptoms, including:3

  • Premature birth (adjusted odds ratio [aOR]: 1.93)
  • Low birth weight (aOR: 2.11)
  • Prenatal tobacco exposure (aOR: 1.41).

A longitudinal Finnish study of 828 newborn infants followed up for 56 months also reported an association between low birth weight and parent-rated symptoms of ADHD.4

Children who were small for gestational age at birth were 3.6-times more likely to have ADHD symptom scores above the clinical cut-off at age 56 months than children of normal birth weight (95% confidence interval [CI] 1.63–7.95; p=0.002).4

Results from a US survey of 2588 children (aged 8–15 years) suggested that maternal cigarette use during pregnancy was significantly associated with childhood ADHD (aOR: 2.4, 95% CI 1.5–3.7; p=0.001).2

Similarly, a study of 356 British children (aged 6–16 years) with ADHD identified maternal smoking during pregnancy as a risk factor for greater hyperactive-impulsive symptom severity.6

Socioeconomic risk factors

A number of international studies have identified socioeconomic factors associated with development of ADHD symptoms. These include:

  • Non-intact family*/single-parent household3,5
  • Paternal history of antisocial behaviour3
  • Maternal depression3
  • Lower maternal education5
  • Lower social class6
  • Households of social welfare recipients5
  • Young maternal age at birth of the target child.3

*Child not living with both biological parents

Environmental contaminants

Environmental exposure to lead has been identified as a risk factor for ADHD in several studies:

  • In the US National Health and Nutrition Examination Survey, high blood lead concentrations in children (aged 8–15 years, n=2588) were significantly associated with ADHD (aOR: 2.3; 95% CI 1.5–3.8; p=0.001)2
  • Data from the New England Children’s Amalgam Trial suggested that children (aged 6–10 years) with blood lead levels of 5–10 μg/dL had lower scores in tests of IQ, acheivement, attention and working memory than children with levels of 1–2 μg/dL (p=0.03)7
  • Low-level lead exposure was associated with higher ADHD scores in a study of 246 African American inner-city children at age 7.5 years.1

ADHD aetiology may result from complex interactions between genetic and environmental influences8-14

Gene–environment interactions have been reported for ADHD (or component symptoms of inattention, hyperactivity and impulsivity), and may explain individual differences observed in response to environmental risk factors.

Combinations of polymorphisms in certain genes and environmental factors may be associated with an increased likelihood of some ADHD symptoms, for example, dopaminergic genes and maternal smoking, alcohol use or stress during pregnancy.8-10,12

In adults:

  • Dopaminergic genes and stressful life events15
  • Serotonergic genes and adverse childhood environment.16

Combinations of specific polymorphisms and environmental risk factors that may increase the likelihood of ADHD symptoms

a) Children and adolescents


b) Adults


  1. Chiodo LM, Jacobson SW, Jacobson JL. Neurodevelopmental effects of postnatal lead exposure at very low levels. Neurotoxicol Teratol 2004; 26: 359-371.
  2. Froehlich TE, Lanphear BP, Auinger P, et al. Association of tobacco and lead exposures with attention-deficit/hyperactivity disorder. Pediatrics 2009; 124: e1054-e1063.
  3. Galéra C, Côté SM, Bouvard MP, et al. Early risk factors for hyperactivity-impulsivity and inattention trajectories from age 17 months to 8 years. Arch Gen Psychiatry 2011; 68: 1267-1275.
  4. Heinonen K, Räikkönen K, Pesonen AK, et al. Behavioural symptoms of attention deficit/hyperactivity disorder in preterm and term children born small and appropriate for gestational age: a longitudinal study. BMC Pediatr 2010; 10: 91.
  5. Hjern A, Weitoft GR, Lindblad F. Social adversity predicts ADHD-medication in school children–a national cohort study. Acta Paediatr 2010; 99: 920-924.
  6. Langley K, Holmans PA, van den Bree MB, et al. Effects of low birth weight, maternal smoking in pregnancy and social class on the phenotypic manifestation of Attention Deficit Hyperactivity Disorder and associated antisocial behaviour: investigation in a clinical sample. BMC Psychiatry 2007; 7: 26.
  7. Surkan PJ, Zhang A, Trachtenberg F, et al. Neuropsychological function in children with blood lead levels <10 microg/dL. Neurotoxicology 2007; 28: 1170-1177.
  8. Brookes KJ, Mill J, Guindalini C, et al. A common haplotype of the dopamine transporter gene associated with attention-deficit/hyperactivity disorder and interacting with maternal use of alcohol during pregnancy. Arch Gen Psychiatry 2006; 63: 74-81.
  9. Grizenko N, Fortier ME, Zadorozny C, et al. Maternal Stress during Pregnancy, ADHD Symptomatology in Children and Genotype: Gene-Environment Interaction. J Can Acad Child Adolesc Psychiatry 2012; 21: 9-15.
  10. Kahn RS, Khoury J, Nichols WC, et al. Role of dopamine transporter genotype and maternal prenatal smoking in childhood hyperactive-impulsive, inattentive, and oppositional behaviors. J Pediatr 2003; 143: 104-110.
  11. Martel MM, Nikolas M, Jernigan K, et al. The dopamine receptor D4 gene (DRD4) moderates family environmental effects on ADHD. J Abnorm Child Psychol 2011; 39: 1-10.
  12. Neuman RJ, Lobos E, Reich W, et al. Prenatal smoking exposure and dopaminergic genotypes interact to cause a severe ADHD subtype. Biol Psychiatry 2007; 61: 1320-1328.
  13. Nikolas M, Friderici K, Waldman I, et al. Gene x environment interactions for ADHD: synergistic effect of 5HTTLPR genotype and youth appraisals of inter-parental conflict. Behav Brain Funct 2010; 6: 23.
  14. Retz W, Freitag CM, Retz-Junginger P, et al. A functional serotonin transporter promoter gene polymorphism increases ADHD symptoms in delinquents: interaction with adverse childhood environment. Psychiatry Res 2008; 158: 123-131.
  15. Sánchez-Mora C, Richarte V, Garcia-Martínez I, et al. Dopamine receptor DRD4 gene and stressful life events in persistent attention deficit hyperactivity disorder. Am J Med Genet B Neuropsychiatr Genet 2015; [Epub ahead of print].
  16. Jacob CP, Nguyen TT, Dempfle A, et al. A gene-environment investigation on personality traits in two independent clinical sets of adult patients with personality disorder and attention deficit/hyperactive disorder. Eur Arch Psychiatry Clin Neurosci 2010; 260: 317-326.

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