Environmental Contaminants in Breast Milk

Krista Nickerson, CNM, MSN


J Midwifery Womens Health. 2006;51(1):26-34. 

In This Article

Breastfeeding Exposure to POPs in Infants: Pharmacokinetics and Body Burden

The pharmacokinetics of POP transfer from mother to infant via breastfeeding is a complex process that is strongly influenced by a particular chemical characteristic of all POPs—their distinct affinity for fat. POPs are lipophilic by nature. When consumed, they bioconcentrate in adipose tissue, and because of their long half-life, POPs accumulate with age and exposure. These chemicals remain in fat storage, making up the organism's lifetime body burden, while minute amounts circulate in serum. Excretion of POPs occurs either very slowly through stool or more quickly through lactation. Figure 1 illustrates the pathway of POPs excretion in the body of a lactating woman.[15] The half-life of dioxins in adults is approximately 4.2 to 5.6 years.[13] Although pregnancy exposes the fetus to minor amounts of POPs carried in serum and transferred via the placenta, a more significant exposure occurs through breastfeeding.[14,16]

Pathways of transition for persistent organic pollutants in lactating women. Adapted with permission from Jensen.[15] (Figure by C. Byrne).

Lactational physiology exerts a unique influence on the kinetics of POPs. When a woman begins lactating, her fat stores are mobilized to efficiently excrete lipids and their trailing POP partners in breast milk. She effectively transfers her own body burden of pollutants to her newborn. The lipid content in breast milk may have concentrations of POPs 10 times higher than lipids of ordinary food.[17]

Levels of POPs in human milk formula are minimal to none. Although formula is derived mostly from cow's milk, the milk fat is replaced by vegetable oils, which are usually free of these contaminants. In a study of 246 preschool children in Michigan, the serum PCB level in formula-fed children was 0.3 ± –0.7 ng/mL, compared to 5.1 ± 3.9 ng/mL in children who were breastfed for at least 6 months.[17] Postnatal exposure via breastfeeding is the principal determinant of body burden levels during early childhood, is significantly correlated with maternal levels, and shows a dose-dependent relationship based on length of breastfeeding.[16,17,18]

Several different pharmacokinetic models of estimating infant body burden due to breastfeeding have been proposed.[17,19] Some models have been used to estimate the extended effect of breastfeeding on infant lifetime body burden[17] or on the toxicologic potential of the body burden.[19] These models include factors such as maternal body burden levels and lactation-dependent changes, milk composition, length of breastfeeding, transfer kinetics, and metabolism of the chemical. The daily dioxin intake of breast-fed infants may be as high as 80-fold higher than in adults.[20] Others have estimated that by adulthood, breastfed individuals will accumulate a dose 3% to 18% higher than individuals who were not breastfed.[21] To the contrary, another model predicts that breastfed and nonbreastfed individual body burdens will eventually equalize by the age of 10.[17] The various methods of producing these estimates have been scrutinized, and they remain merely estimates and best guesses based on the available information.

A mother's body burden of POPs is dependent on several factors. Background exposure is derived mostly from low-level food and water contamination. Important factors for women with normal background exposure (i.e., no acute episodes of high exposure) seem to be age and previous lactation.[22] Age is an indicator of exposure level because the passage of time allows for continued accumulation of pollutants. Older nulliparous women are expected to have higher body burdens. However, previous lactation is associated with lower POP levels in breast milk.[10,22] Researchers have estimated that maternal PCB/dioxin body burden decreases as much as 20% to 70% during 6 months of exclusive breastfeeding.[17,22] Thus, over the course of her childbearing years, a mother will transfer more POPs to her first child, with decreasing amounts to subsequent children.

Geographic location influences body burden of POPs based on proximity to agricultural use of chemicals, waste incineration sites, and other factors. For example, Inuit women have the greatest body burden known to occur from general background environmental exposure, secondary to climate factors and a diet of lipid-rich sea mammals.[23] The accumulation of POPs in the arctic environment, far from their original site of production and use, is via long-distance atmospheric and oceanic transport.[24]

Other determinants of exposure that influence maternal body burden to varying degrees include diet, cigarette smoking, urban living, and occupation.[7] It is generally agreed that food represents the main source (over 90%) of environmental exposure to dioxins and PCBs.[20] Within the diet, animal products (dairy, meat, and fish) appear to contain the highest amounts of dioxins/PCBs, because of their accumulation in fat. Therefore, a vegetarian diet appears to be associated with lower serum dioxin levels.[10] However, short-term dietary regimens with a low PCB/dioxin intake do not reduce breast milk levels.[25] Consumption of freshwater sports fish conveys a higher level of PCBs in breast milk.[22] Cigarette smoking increases levels of DDE, PCBs, and hexachlorobenzene.[7,22,26] Finally, breast milk PCB levels differ according to occupation; students and professionals have higher levels than laborers and farmers.[22] Neither education nor body weight seems to affect PCB or DDT levels[22]; however, weight loss seems to concentrate dioxin levels in body fat.[10]


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