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Rapid changes in organ development and function occur during the neonatal period. During this period the central nervous system is in a rapid growth rate and highly vulnerable to toxic effects of, e.g., lead and methylmercury. Furthermore, the kinetics of many metals is age-specific, with a higher gastrointestinal absorption, less effective renal excretion as well as a less effective blood-brain barrier in newborns compared to adults. Due to their low body weight and high food consumption per kg of body weight, the tissue levels of contaminants can reach higher levels in newborns than in adults. Generally, there is a low transfer of toxic metals through milk when maternal exposure levels are low. However, knowledge is limited about the lactational transport of metals and the potential effects of metals in the mammary gland on milk secretion and composition. There are some data from rodents on the lactational transfer and the uptake in the neonate of inorganic mercury, methylmercury, lead and cadmium. Metal levels in human breast milk and blood samples from different exposure situations can give information on the correlation between blood and milk levels. If such a relationship exists, milk levels can be used as an indicator of both maternal and neonatal exposure. Better understanding of the neonatal exposure, including kinetics in the lactating mother and in the newborn, and effects of toxic metals in different age groups is needed for the risk assessment. Interactions with nutritional factors and the great beneficial value of breast-feeding should also be considered.

Even at the low exposure level of cadmium found in this study population living on farms in southern Sweden, there was an indication of effect on biochemical markers of renal function. Women had higher blood cadmium (BCd) and urinary cadmium (UCd) than men, which can be explained by higher absorption of Cd due to low iron status. In the present study, Cd in pig kidneys could not be used to predict human BCd or UCd even though cereals are a substantial part of both the human and the pig diet. The contribution of Cd from locally produced food to the total dietary intake in humans was relatively low and varied and the intake of Cd did not correlate with BCd or UCd. In contrast, Cd levels in pig kidney were significantly related to Cd levels in feed. However, there was no relationship between the locally produced cereals, constituting the main part of the feed, and Cd in pig kidneys. In pig feed, other non-locally produced ingredients contributed to a large part of the Cd in feed. The Cd in non-locally produced feed ingredients reaches the local circulation via excretion in faeces and application of manure to arable soils and will lead to increased levels in the crops. As indicated by experimental data from animals, neurochemical and neurobehavioral effects during development need to be further explored as sensitive endpoints for cadmium toxicity.