Aflatoxins (AFs) are secondary metabolites of the fungi Apergillus flavus and Aspergillus parasiticus. These moulds are common contaminants of foodstuff, particularly in the tropical regions [1]. Many studies have linked aflatoxin contamination of food with some toxic effects such as liver cancer and immunosupression in various animals and humans [2,3]. Aflatoxin B1, the most potent one, is metabolized into a variety of hydroxylated derivatives (aflatoxin P₁, M₁, B_2a, aflotoxicol) which are less toxic than the parent compound [4], although their presence in food is still a threat to human health [5]. Aflatoxin B₁ has been detected in human foodstuffs in some African countries [6] and correlated with a high incidence of primary liver cancer. In Cameroon, some of our early reports [7–9] have shown the presence of AFB₁ and some of its metabolites in foodstuff and animal feed at levels higher than recommended by the guidelines issued by international regulatory committees [10]. In spite of these studies, the relation between aflatoxin contamination in body fluids and states of some diseases such as cancer and malnutrition is not very obvious because of insufficiency of statistical data in our country. This contamination, in addition to infection by some viruses such as hepatitis B or HIV [11,12], could have serious effects on the quality of health in Cameroon. This study was therefore designed to determine the levels of aflatoxins in foods which are recommended as high protein sources for children, like eggs and milk, and the blood and urine of patients suffering from malnutrition and cancer.

Aflatoxin contamination in various foods is a major threat to the health of exposed people. We detected AFB₁, AFB_2a and AFM₁ in egg samples, thus confirming our earlier reports [7,8]. Apart from AFB_2a which is known to have low toxicity, the two other compounds are highly toxic [19]. This emphasizes the importance of monitoring AFB₁ and its metabolites in poultry products. Overall, the forest region had the highest toxin contamination. Factors such as time of exposure of the hen, rate of formation of metabolites and their rate of transfer to the egg may influence egg contamination, but these factors were not evaluated during this study. It has been reported that contamination of eggs may influence the performance of chick after hatching [20]. Apart from eggs, AFB₁ has also been detected in gizzard and chicken muscle [21].

AFM₁ was also detected in 15.9% of the cow milk samples at levels higher than the recommended maximum (Table 2). This was probably due to the contamination of feed given to the cattle, since it is well known that AFM₁ is usually excreted in milk two days after ingestion of feed contaminated by AFB1 [22]. In addition to the contamination of local milk, contamination has also been found with milk powder and pasteurised milk in various European countries [10,23–25].

Milk from breastfeeding mothers (4.8%) was also contaminated with AFM₁. This implies that children might be regularly exposed to AFM₁ via breast milk or imported processed milk from European countries. Further, AFB₁ has been reported in cord blood of children in Nigeria and Ghana [26], meaning that it crosses the placental barrier from the mother to the foetus. In utero exposure of the foetus to toxins, exposure of children to environmental toxins, and the nutritional status of the infant, are considered critical for growth and risk of disease in early life. Indeed, malnutrition is one of the common problems in developing countries.

The presence of AFB₁ in body fluids of children is a potential risk of impairment of growth during their development, since it is well known that it inhibits protein synthesis [27]. We detected AFB1 in the urine of malnourished children and there seemed to be a link between malnutrition and the presence of AFB₁ in the urine of malnourished children (P < 0.05 Dunnett; Table 4). It is possible that the presence of the toxin is a reflection of food habits of the mothers whose knowledge, attitudes and practices with respect to food may vary considerably.

Indeed, research on humans in Benin and Togo showed a dose-response relationship between exposure to aflatoxin, degree of stunting and underweight in children under five years of age; the study population was exposed to aflatoxin, with 99% of the children having serum aflatoxin-albumin adducts [28]. Further, many researchers in African countries have reported a strong association between malnutrition and the presence aflatoxin in body fluids from children [2], although studies with periurban children and children hospitalised for kwashiokor in South Africa did not find any aflatoxin contamination [29]. As a consequence of the known effect of aflatoxin on protein synthesis, aflatoxin in body fluids of children could be a modulating factor on the rate of recovery from protein malnutrition, although it has not been shown to be responsible for the development of the condition. Further, it has been suggested that aflatoxin reduces the nutritional capacity of food by interfering with metabolic processes [30]. Species differences in the acute and chronic toxicity of AFB1 have been documented in animal, with females showing greater resistance to the toxin [31]. Our results seem to show a greater proportion (10/21 males and 6/21 females) of urine samples from male children contaminated more than samples from female children with kwashiorkor and marasmic kwashiorkor (Table 4), Since we did not follow the daily intake of aflatoxins in food consumed by male and female children, it cannot be concluded that our results corroborate the observations made in animals. Therefore, sex differences related to aflatoxin toxicity in human is still to be proven.

Exposure to AFB₁ from early age could be a predisposing factor for primary liver cancer. Indeed, it is well known that aflatoxins, viral hepatitis, alcohol, and cigarette are high risk factors for cancer development [5]. Our results show that 63.9% of samples from primary liver cancer patients were positive for AFB₁ while 69.4% were positive for HbsAg. We did not find any linkage between contamination with AFB₁ and infection with HBV, but this is not surprising because the two factors are independently introduced into the subject. However, since both aflatoxin and HBV have an effect on the liver, there is need to investigate the effect of the food contamination reported here on the evolution of HBV pathology, especially the possible additive or synergistic effects, and the possible contribution of other environmental factors [32].

In conclusion, aflatoxins seem to be present in foods recommended for children like eggs and milk, at levels above recommended thresholds. A high prevalence of contamination was found in the urine and blood of malnourished children with kwashiorkor and marasmic kwashiorkor; people with primary liver cancer also had a high prevalence of contamination with aflatoxin and infection with HBV. It is necessary to investigate if aflatoxin has an additive or synergistic effect on the pathology of HBV.