Scientists from OHSU (Oregon Health & Science University) Doernbecher Children’s Hospital have published the first ever study to confirm a causal link between blood lead exposure and attention deficit hyperactivity disorder (ADHD) in humans
While previous studies have associated lead blood levels with ADHD, this latest study is the first to confirm previous hypotheses that exposure to lead in miniscule amounts of less than 10 parts per billion increases symptoms in some individuals with ADHD.
This research is valuable to the scientific community as it bridges genetic and environmental factors and helps to illustrate one possible route to ADHD
said principal investigator Joel Nigg, PhD.
Further, it demonstrates the potential to ultimately prevent conditions like ADHD by understanding how genes and environmental exposures combine
Nigg is director of OHSU’s ADHD & Attention Research Program, director of the Division of Psychology at OHSU Doernbecher Children’s Hospital and professor of psychiatry and behavioural neuroscience at OHSU’s School of Medicine.
To conduct this research, Nigg and colleagues evaluated lead blood level in 386 healthy children aged 6 to 17. Half of the children had been carefully diagnosed with ADHD. All children were within the safe lead exposure range as defined by the Centers for Disease Control and Prevention, and the blood lead level in the sample was typical of the national US population of children.
Their analysis showed a heightened causal link between lead exposure and ADHD symptoms – particularly hyperactivity-impulsivity – in those with the HFE C282Y gene mutation, which is present in approximately 10 per cent of US children.
Because the C282Y gene helps to control the effects of lead in the body and the mutation was spread randomly in the children, the findings of our study are difficult to explain unless lead is, in fact, part of the cause of ADHD, not just an association
The study also found that lead effects were more robust in males, which is consistent with previous research specific to neuro-developmental conditions and gender. Children without HFE C282Y mutations showed amplified symptoms as lead exposure increased, but not as consistently.
The scientists said the findings do not indicate that lead is the only cause of ADHD symptoms, nor that lead exposure will guarantee an ADHD diagnosis; rather, the study demonstrates that environmental pollutants, such as lead, do play a role in the explanation of ADHD.
Despite US government regulations that drastically reduced environmental exposure to lead, the neurotoxin is still found in common objects such as children’s toys and costume jewellery. It also continues to be ingested in small amounts via water from ageing pipes, as well as contaminated soil and dust. At very high levels, lead poisoning may result in seizures, coma or even death. However, long term, lower-level exposures are a more common health threat, particularly in children.
Our findings put scientists one step closer to understanding this complex disorder so that we may provide better clinical diagnoses and treatment options and, eventually, learn to prevent it