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.
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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.
Dr. Susan D. Swick
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.
Behavior
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.