To determine whether children with language delays are more likely to
ha c e been exposed to cocaine in utero than children with normal lang
uage development, a case-control study was undertaken. Based on routin
e office screening in our primary-care clinic over a 1-year period, we
identified 29 consecutive children, aged 24 to 48 months, as language
-delayed. They were compared with an approximate 2:1 match of children
without language delay who had been seen in the clinic on the same da
ys and who were of similar age. There was more reported cocaine use du
ring pregnancy (six of 29, 21%) among the language-delayed children th
an among the controls (five of 71, 7%). This difference is statistical
ly significant (P < 0.05, chi(2) = 3.92; odds ratio = 3.4 +/- 2.2). Di
scriminant analysis revealed that both cocaine and nicotine exposure w
ere associated with delayed language development - with an unexpected
negative, i.e., an antagonistic, protective, interactive effect (F[3,9
6] = 4.66, R(2) = 12.7%, P<.005); neither gender nor caretaker contrib
uted to language development in this sample. These results suggest tha
t children with language delay detected in a clinical setting are more
likely to have been exposed in utero to cocaine than children with no
rmal language development. Prenatal cocaine exposure should be a risk
factor in monitoring development in children.