Postnatal Exposure to the Drug in Susceptible Infants and Children Could Be Causal in Many Cases of ASD
A team of North Carolina researchers recently reviewed the safety profile of paracetamol (acetaminophen) use for infants and children. Acetaminophen is the active ingredient for the over-the-counter drug Tylenol, which treats minor pain and reduces fevers. Since the 1970s, the drug has been considered safe to use during pregnancy and childhood. However, recently acetaminophen’s claim of safety has been questioned. In the current review, the researchers describe how the drug can damage a developing child’s body, explaining that a fraction of acetaminophen is converted into the highly toxic metabolite, N-acetyl-p-benzoquinone imine (NAPQI). In healthy individuals, NAPQI becomes neutralized by glutathione. But for infants or children dealing with oxidative stress, their glutathione levels become depleted, leading to increased production of NAPQI. Under this condition, NAPQI reacts with a wide range of proteins, causing permanent damage to those proteins and resulting in cell toxicity. While most children will metabolize acetaminophen without problem, a number of children who have oxidative stress are at risk for acetaminophen-induced toxicity. This toxicity can lead to neurodevelopmental disorders, especially autism, in susceptible children. The review’s authors point out that the risk of injury from the drug comes down to two factors: 1) the exposure amount of acetaminophen and 2) the amount of oxidative stress present at the time when exposure to acetaminophen occurs. In the end, the review states that based on the evidence examined, including temporal relationships, data from laboratory animal studies, and other correlations, it can be concluded that oxidative stress puts some infants and children at risk for acetaminophen-induced neurodevelopmental injury. Additionally, the review claims that postnatal exposure to acetaminophen is responsible for many, if not most, cases of autism in at-risk children.
