Health Outcomes of POP Exposure in Infants
Extensive laboratory and animal research has shown that POPs have a significant effect on the biochemical processes and function of several organ systems. Although these studies are immensely important to the science of toxicology, this review focuses on human studies only. Because human research is more methodologically and ethically complex, fewer studies are available, and their results are harder to interpret. In general, the question is not whether there are adverse effects, but rather, are adverse effects occurring at the existent levels of exposure? For example, although minor changes in motor function or memory may be insignificant to the individual child, the idea that a portion of children in the general population are noted to be affected by using insensitive methods of detection is worrisome. All of the evidence provided here concerns levels of contaminants that are found in human populations at normal exposure levels.
Infancy is a unique developmental period in the human life span. During this stage, the immunologic, neurologic, and reproductive systems are functionally immature, and the infant undergoes rapid tissue growth and development. In addition, this development necessitates a larger quantity of calories per body weight and increased fat consumption via breast milk or formula. These factors create potential for significant systemic effects, whether beneficial or detrimental. The research on health outcomes of perinatal exposure to POPs has focused on the endocrine, reproductive, immune, and neurologic systems.
It is important to acknowledge the difficulty in distinguishing effects that may be associated with in utero toxic exposure versus those that are from breastfeeding. In utero exposure to POPs does occur to a much lesser degree. However, because of increased vulnerability during fetal development, the impact of the smaller exposures during pregnancy may surpass the infinitely larger exposure to POPs in breast milk. The research involving the health effects of POP exposure through breastfeeding does not always control for the possibility of teratogenic exposure to POPs during gestation. These differences will be elucidated where studies have distinguished between the two.
Preliminary evidence regarding overall growth has shown that in utero exposure to PCBs may cause low birth weight; however, there is contradictory evidence regarding breastfeeding exposure and weight gain in infancy and early childhood.[14,28] Several studies have looked at pubertal growth and perinatal exposure to PCBs and DDE.[29,30] All of them have found that prenatal exposure to PCBs may cause an increase in body size at puberty for girls. However, no relationship was seen with lactational exposure.
Less evidence is available on POPs and reproductive outcomes. Animal studies have clearly linked PCBs and dioxins to reduced sperm count and fertility, endometriosis, and altered sexual development and behavior. However, very few human studies have been completed. Perinatal exposure to PCBs and DDE did not seem to affect pubertal development, as measured by Tanner stages and age of menarche.[29,30] On the other hand, Michels-Blanck et al. completed a study of 327 girls whose mothers, affected by an industrial accident, were exposed to high levels of PBBs through animal and dairy products. It was found that perinatal PBB exposure led to a decrease in the age of menarche and earlier pubic hair development in the girls born to mothers who were exposed. The study was unable to distinguish prenatal from postnatal exposure. The postulated mechanism for such effects is via endocrine disruption and/or estrogenic activity of the various POPs.
POPs may also disrupt the endocrine process of lactation itself. Gladen and Rogan and Rogan et al. investigated the role of DDE and PCBs on the duration of lactation in three communities in North Carolina and one community in Mexico. Levels of DDE and PCBs were measured in the milk of lactating women and compared with their reported duration of lactation. Higher levels of PCBs and DDE in breast milk were associated with decreased duration of lactation, despite adjustments for potential confounders and biases. The authors concluded that DDE and PCBs may affect women's ability to lactate, suggesting that the chemicals' estrogen-like effects may inhibit the process. In another study, milk volume was found to be inversely related to PCB body burden.
Additional preliminary evidence indicates that perinatal exposure to PCBs and dioxins may disrupt thyroid hormone regulation; however, the data are contradictory.[30,34] Inconsistencies may be related to different methods of study, as well as the presence of multiple confounding factors. Koopman-Esseboom et al. studied 105 maternal-infant pairs and found that higher levels of dioxins and PCBs correlated with significantly lower plasma levels of maternal total triiodothyronine and total thyroxine and with higher plasma levels of TSH in the infants in the second week and third month after birth. However, direct, isolated measurements of thyroid hormone levels may not be the most sensitive indicator of a perturbation of thyroid hormone metabolism. It is well documented that thyroid hormone regulation has a profound effect on neurologic development; therefore, any disturbance has the potential for adverse effects.
The research concerning neurodevelopmental effects of PCB and dioxin exposure is both more extensive and more consistent than research on growth and endocrine development. Although breastfeeding exposure to PCBs and dioxins occurs to a much greater degree than prenatal exposure, it appears that prenatal exposure has a more measurable effect on neurodevelopmental outcomes. Prenatal exposure to PCBs has been associated with hypotonicity and hyporeflexia in newborns; poorer psychomotor performance at 3, 6, and 12 months; poorer cognitive functioning at 42 months; poorer mental and motor development between 7 and 42 months; and poorer short-term memory function at 4 years. Several of these studies had inconsistent results and did not find significant effects in every area or age group tested. Meanwhile, despite the high PCB and dioxin levels transferred via breast milk, breastfeeding seemed to have a beneficial effect on neurologic status compared with formula feeding.[36,38] Other factors present in breast milk may have a protective effect on normal neurologic development. However, when comparing only breastfed infants and ignoring their formula-fed counterparts, the deleterious effects of higher levels of POPs in breast milk reappears. Walkowiak et al. found that mental and motor development between 7 and 42 months of age has a significant negative association with PCB concentration in early human milk but not in cord blood samples.
There are several limitations to the research on neurodevelopment scores. One particular difficulty in studying older children is that factors such as the home environment and maternal IQ become more significant variables that affect development as a child ages.[36,39] Both human and animal studies have demonstrated that POPs and other contaminants rarely occur individually, and the effects of these chemicals are quite complex, as are the neurodevelopmental processes of humans. Global functioning tests may not be able to distinguish deficits of one particular domain, because they will be masked by the inability of the test to discriminate between global functioning and specific cognitive functions.
There are very few studies concerning perinatal exposure to POPs and their effect on the immune system. Moreover, the immune-supporting properties of breast milk are well known and have a beneficial effect on infants, which may mask any harmful influence of POPs. Weisglas-Kuperus et al. investigated the effect of prenatal and postnatal PCB levels on the prevalence of infectious diseases. They measured humoral immunity to antibodies after vaccination and measured immunologic markers in children at 42 months. Results demonstrated that prenatal PCB exposure was associated with lower antibody levels to mumps and measles after vaccination and significant changes in T-cell markers, indicating a greater susceptibility to infectious diseases. High current PCB levels were associated with a higher prevalence of recurrent middle ear infections and chicken pox and lower prevalence of allergic reactions. Increased dioxin levels were associated with higher prevalence of coughing, chest congestion, and phlegm. It is of interest that the negative effect of high postnatal PCB level was counteracted by the positive effect of longer duration of breastfeeding. DeWailly et al. measured levels of 10 PCB congeners and 8 different organochlorine pesticides or metabolites in the breast milk of 213 Inuit women and the chemicals' relation to serum immunologic parameters and occurrence of otitis media in the women's infants. The study found that immunologic parameters did not differ between breast and formula-fed infants, nor was there an association between the milk levels of the pollutants that were assessed and immunologic parameters in the infants. On subanalysis, DDE and hexachlorobenzene levels in breast milk were positively associated with occurrence of otitis media within the first year of life.
There is no evidence implicating perinatal exposure to POPs to carcinogenic effects, yet the issue warrants mentioning. All these agents are known or suspected carcinogens in the laboratory. Although any estimate of long-term risk to the child involves making assumptions, at least one analysis has tried to calculate the increased risk of cancer due to PCB exposure via breastfeeding. Meanwhile, epidemiologic or long-term studies of POPs in breast milk assessing the subsequent incidence of cancer have been conducted. Exposure to breast milk in infancy does not appear to be related to adult breast cancer risk. However, breastfeeding is associated with a decreased rate of premenopausal breast cancer for the mother. One factor may be that the breastfeeding women rid their bodies of POPs, thus providing some protection against the carcinogenic qualities of these pollutants.
J Midwifery Womens Health. 2006;51(1):26-34. © 2006 Elsevier Science, Inc.
Cite this: Environmental Contaminants in Breast Milk - Medscape - Jan 01, 2006.