presence of aflatoxins in smoked-dried fish sold in abeokuta, ogun ...

geographical location. These data suggest that aflatoxin may inhibit growth in West African
children (Gong et al., 2002).
In a small study of the presence of aflatoxin in cord blood in Ibadan, Nigeria, a significant
reduction in birth weight was found in jaundiced neonates, who had significantly higher serum
aflatoxin concentrations compared with babies without jaundice (Abulu et al., 1998).
In a study to investigate whether aflatoxins contribute to the occurrence of jaundice in Ibadan,
blood samples were obtained from 327 jaundiced neonates and 60 non-jaundiced controls.
Aflatoxins were detected in 24.7% of jaundiced neonates and in 16.6% of controls. Analysis of
the data indicated that either glucose-6-phosphate dehydrogenase deficiency or serum aflatoxin
are risk factors for neonatal jaundice; odds ratios were significantly increased: 3.0 (95% CI, 1.3–
6.7) and 2.7 (95% CI, 1.2–6.1), respectively (Sodeinde et al., 2005).
Aflatoxins were detected in 14 of 64 (37.8%) cord blood samples from jaundiced neonates
compared with 9 of 60 (22.5%) samples from non-jaundiced control babies in another study in
Nigeria, but the difference was not statistically significant (Ahmed et al., 1995).
Aflatoxins were detected in 37% of cord blood samples in a study of 125 pregnancies in rural
Kenya, with 53% of maternal blood samples being aflatoxin-positive. There was no correlation
between aflatoxins in maternal and cord blood. A significantly lower mean birth weight of
infants born to aflatoxin-positive mothers was recorded for female babies, but not for males (De
Vries et al., 1989).
In cord blood collected from 625 babies in Nigeria, aflatoxins were detected in 14.6% of the
samples. There was no significant difference in birth weight between the groups positive or
negative for aflatoxins (Maxwell et al., 2004).
In a study of the presence of the imidazole ring-opened form of aflatoxin B1–DNA adducts in
placenta and cord blood, 69 of 120 (57.5%) placentas contained the adduct at 0.6–6.3 µmol/mol
DNA and 5 of 56 (8.9%) cord blood samples contained the adduct at 1.4–2.7 µmol/mol DNA.
The results indicate that transplacental transfer of aflatoxin B1 and its metabolites to the progeny
is possible (Hsieh, 2003).
A random sampling of semen from adult men, comprising 50 samples collected from infertile
men and 50 samples from fertile men from the same community in Nigeria, revealed the
presence of aflatoxin B1 in 40% of samples from infertile men compared with 8% in fertile men.
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