IARC MONOGRAPHS ON THE EVALUATION OF CARCINOGENIC ...

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IARC MONOGRAPHS VOLUME 82
but in most studies, various confounders were not controlled for and exposure levels
were not investigated.
Aflatoxins have been reported to occur in up to 40% of samples of breast milk
collected from women in tropical Africa (Hendrickse, 1997) (see also Section 1.3.3(b)).
Concentrations of aflatoxin M 1 were measured in breast milk of women from
Victoria (Australia) and Thailand as a biomarker for exposure to aflatoxin B 1. Aflatoxin
M 1 was detected in 11 of 73 samples from Victoria (median concentration,
0.071 ng/mL) and in five of 11 samples from Thailand (median concentration,
0.664 ng/mL) (El-Nezami et al., 1995).
In a survey of the occurrence of aflatoxins in mothers’ breast milk carried out in Abu
Dhabi and involving 445 donors, 99.5% of samples contained concentrations of aflatoxin
M 1 ranging from 2 pg/mL to 3 ng/mL (Saad et al., 1995).
Maxwell (1998) reviewed the presence of aflatoxins in human body fluids and
tissues in relation to child health in the tropics. In Ghana, Kenya, Nigeria and Sierra
Leone, 25% of cord blood samples contained aflatoxins, primarily M 1 and M 2, in variable
amounts (range for aflatoxin M 1: 7 ng/L–65 μg/L).
Of 35 cord serum samples from Thailand, 17 (48%) contained aflatoxin concentrations
of 0.064–13.6 nmol/mL (mean, 3.1 nmol/mL). By comparison, only two (6%) of
35 maternal sera obtained immediately after birth of the child contained aflatoxin (mean,
0.62 nmol/mL). These results demonstrate transplacental transfer and indicate that
aflatoxin is concentrated by the feto-placental unit (Denning et al., 1990).
A study of 480 children (aged 1–5 years) in Benin and Togo examined aflatoxin
exposure in relation to growth parameters. Mean concentrations of aflatoxin–albumin
adducts in the blood were 2.5-fold higher in fully weaned children than in those who
were still partially breast-fed. There was a strong negative correlation between aflatoxin–albumin
adduct levels in the blood and both height-for-age (stunting) and weightfor-age
(being underweight) compared with WHO reference population data after adjustment
for age, sex, weaning status, socioeconomic status and 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 nonjaundiced
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., 1995).