though ADHD is correlated with smoking du ring pregnancy, some of this association
reflects common genetic risk. A minority of c ases may be related to reactions to aspects of
diet. There may be a history of child abuse, neglect, multiple  foster placements, neurotoxin
exposure (e.g., lead), infectio ns (e.g., encephalitis), or alcohol exposure in utero. Exposure
to environmental toxicants has been correlat ed with subsequent ADHD, but it is not
known whether these associations are causal.
Genetic and physiological. ADHD is elevated in the firs t-degree biological relatives of
individuals with ADHD. The heritability of AD HD is substantial. While specific genes
have been correlated with ADHD, they are ne ither necessary nor sufficient causal factors.
Visual and hearing impairments, metabolic abnormalities, sleep  disorders, nutritional de-
ficiencies, and epilepsy should be considered as possible influences on ADHD symptoms.
ADHD is not associated with specific physic al features, although  rates of minor phys-
ical anomalies (e.g., hypertelorism, highly arched palate, low-set ears) may be relatively
elevated. Subtle motor delays and other neur ological soft signs may occur. (Note that
marked co-occurring clumsiness and motor delays should be coded separately [e.g., de-
velopmental coordina tion disorder].)
Course modifiers. Family interaction patterns in ea rly childhood are unlikely to cause
ADHD but may influence its course or contri bute to secondary development of conduct
problems.
Culture-Related Diagnostic Issues
Differences in ADHD prevalence rates across re gions appear attributable mainly to differ-
ent diagnostic and methodological practices. However, there also may be cultural varia-
tion in attitudes toward or interpretations of children’s behaviors. Clinical identification