Lead poisoning is a well-established cause of serious and permanent neurological, cognitive, and behavioral problems, particularly in exposed children.

Children can be exposed to lead from ingesting paint chips in their homes, when old paint is scrapped from the exterior of houses or bridges, and through the water they drink. The damage caused by lead poisoning was first recognized in the United States in the early 20th century, although lead was added to gasoline and paint until the 1970’s. Since then, regulations for lead in consumer products have become increasingly strict, and the Centers for Disease Control and Prevention’s definition of a toxic lead level has shifted from 60 micrograms/deciliter (mcg/dL) in 1970 to 5 mcg/dL in 2012. In many communities, removing lead paint up to the height of a young child is a requirement whenever an older home is sold.

Unfortunately, these regulations did not protect the families in Flint, Michigan from being exposed to high levels of lead when a change in water supply and inadequate water treatment allowed lead to enter the system from decaying water pipes. It is worth reviewing what is known about the short- and long-term consequences of lead exposure, and what lies ahead for the children of Flint.

Lead is a naturally occurring element that is not metabolized, but rather absorbed, distributed to tissues, and excreted. Lead can be inhaled (with 100% absorption) and introduced through the GI tract (with about 70% absorption in children and 20% absorption in adults). GI absorption is enhanced by calcium or iron deficiency, both conditions that are relatively common, especially in poor children and can lead to pica (or eating of non-nutritious materials), further increasing the chances of lead exposure. Absorbed lead is distributed to blood (for 28-36 days), soft tissue, including the nervous system (40 days), and to bone (where it lasts for over 25 years). Blood that is retained in growing bones can be mobilized during periods of physiologic stress (such as illness, injury, or pregnancy), meaning children exposed to lead during a period of rapid bone growth are at long-term risk for acute lead poisoning from their endogenous reservoir without a new exposure. What lead is not retained by tissues is excreted by the kidneys, with adults retaining about 1% of absorbed lead, while children younger than 2 years retain over 30% of absorbed lead. So children, especially toddlers, have a greater likelihood to absorb lead from the GI tract and to retain lead in their tissues, both due to active mineralization of bone and the permeability of the blood brain barrier, primarily in children under 3 years old. This is why we are addressing what will happen to the children of Flint and not to all the residents of Flint.

Lead competitively inhibits interactions between cations and sulfhydryl groups, which are present in most human biochemical reactions. This leads to irreversible cell damage and often cell death, especially within the central nervous system. Lead exposure is associated with particular dysfunction within dopaminergic pathways within the brain, and has been associated in a dose-dependent fashion with decreased prefrontal gray matter volume. Lead poisoning also has hematologic consequences (anemia), renal consequences (interstitial nephritis), gastrointestinal symptoms (vomiting, constipation), and endocrine consequences (reversible inhibition of Vitamin D metabolism and permanently short stature). But the CNS consequences of lead exposure are particularly devastating, as they appear to have no threshold and are permanent. Their incidence is the driving force for the CDC’s lowering of the official toxic lead level and the public health efforts to screen children and educate parents about the risk of lead exposure.

So what do these serious consequences look like? People with severe lead intoxication (blood lead levels greater than 70 mcg/dL) typically present with signs of acute encephalopathy (headache, vomiting, seizures, or coma) and require intensive medical management including chelation therapy. More typically, exposed children have low but accumulating levels of lead and present with nonspecific symptoms, including lost appetite, fatigue, irritability, and insomnia, which gradually worsen.


High levels of impulsivity, aggression, and impaired attention are the prototypical sequelae of lead poisoning (following recovery from the acute intoxication). Multiple studies have demonstrated these high levels of aggressive and impulsive behaviors in preschoolers who were exposed to lead, and these behaviors appear to continue into adolescence and adulthood. Indeed, one study found that compared with children with the lowest measurable blood lead levels (0.2-0.7 mcg/dL), those children who were in the next two quartiles had seven and twelve times the odds of meeting diagnostic criteria for conduct disorder.1 There have even been studies which correlated atmospheric lead levels (when leaded gasoline was common) with crime rates 20 years later, which supported an association between childhood lead exposure and adult criminal activity.2-4.

Multiple studies have demonstrated higher rates of inattention, distractibility, and impulsivity in lead-exposed children than would be expected given the prevalence of attention-deficit/hyperactivity disorder (ADHD) in the general population. The incidence of these symptoms goes up in a dose-dependent fashion and appears to have no threshold (so they occur at even the lowest measurable blood lead levels). In a 2006 study of nearly 5,000 children between ages 4-15 years, those with blood lead levels greater than 2 mcg/dL (still below the level the CDC deems toxic) were four times more likely to be carrying a diagnosis of ADHD and be on stimulant medication than their peers with blood lead levels less than 0.8mcg/dL.


Closely related to impulse control and attention, the cognitive domains of intelligence and executive function are clearly damaged by lead exposure. Poor performance on tasks requiring focus, cognitive flexibility, and inhibition of automatic responses was directly associated with higher blood lead levels in a group of preschoolers with levels between 0 and 13 mcg/dL.5

IQ has been found to be so consistently diminished by increasing blood lead levels that it is used as an overall index of neurodevelopmental morbidity of lead exposure, leading to the CDC’s adoption of a lower standard definition of toxic lead levels. Even very low blood lead levels are associated with decrements in IQ: children with blood lead levels less than 7.5 mcg/dL lost an average of 3 IQ points for every 1 mcg/dL increase in blood lead levels.6 In a study of 57,000 elementary school students in 2009, Miranda et al. found that those who had a blood lead level of 4 mcg/dL at 3 years old were significantly more likely to be diagnosed with a learning disability in elementary school. Another study of 48,000 children who had a blood lead level of 5 mcg/dL were 30% more likely to fail third grade reading and math tests than their peers without measurable lead levels.

Speech and language

More recent studies have demonstrated that children with higher bone lead concentrations had poorer performance on several language-processing measures, suggesting that childhood lead exposure damages language processing and function as the young people grow. These deficits in language processing can make social development and self-regulation much more challenging in adolescence, and make school and work settings much more challenging. These findings also have implications for the utility of psychotherapy, a language-based treatment, for the other behavioral problems of lead exposure.

Motor skills

Several recent studies have assessed both fine and gross motor skills in lead-exposed children. Findings have demonstrated that balance, coordination, gross motor and fine motor skills all appear to be compromised in a dose-dependent fashion by childhood lead exposure. These findings suggest that not only are children at greater risk for accident and injury through childhood and into adulthood, a risk already increased by their compromised attention and impulse control. But they also are likely to be physically clumsy, compromising an opportunity to cultivate strengths or experience mastery when cognitive tasks may prove frustrating for them.

With deficits in such fundamental cognitive, motor, and behavioral processes, exposed children are clearly vulnerable to more than ADHD, conduct disorder, and learning disabilities. These struggles may lead to secondary vulnerabilities to anxiety or mood symptoms or substance abuse as these children grow into teenagers who face frustration at every turn. In addition to treatment for their deficits in attention and executive function, these children will ideally receive specialized supports in school and at home, to be able to master cognitive tasks, manage new social circumstances and make friends, discover their interests and talents, and generally stay on their best developmental trajectories. Lastly, the specific consequences of lead exposure will vary for any individual child, so parents will have to deal with the uncertainty of their child’s behavior and development over many years. Clearly, the children of Flint face a long road that has been substantially impacted by their lead exposure. The only good that can come from the exposure in Flint is to heighten efforts to ensure that it never happens again.

1. Environ Health Perspect. 2008 Jul;116(7):956-62 .

2. Environ Res. 2000 May;83(1):1-22 .

3. Environ Res. 2007 Jul;104(3):315-36 .

4. Arch Pediatr Adolesc Med. 2001 May;155(5):579-82 .

5. Dev Neuropsychol. 2004;26(1):513-40 .

6. Environ Health Perspect. 2005 Jul;113(7):894-9 .

Dr. Swick is an attending psychiatrist in the division of child psychiatry at Massachusetts General Hospital, Boston, and director of the Parenting at a Challenging Time (PACT) Program at the Vernon Cancer Center at Newton (Mass.) Wellesley Hospital. Dr. Jellinek is professor of psychiatry and of pediatrics at Harvard Medical School, Boston.


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