Intake, Fecal Excretion, and Body Burden of Polychlorinated Dibenzo-p-dioxins and Dibenzofurans in Breast-Fed and Formula-Fed Infants

Abstract

To assess toxicokinetics of polychlorinated dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs), oral intake and fecal excretion were measured in two breast-fed infants and one formula-fed infant during the 1st y of life. The intake of these compounds was up to 50 times higher in the breast-fed infants. In these children, fecal excretion of the main tetra- to hexachlorinated congeners was less than 9% of the intake at age of 1 and 5 mo, indicating almost complete intestinal absorption during breast-feeding. In contrast, distinctly higher fecal excretion rates were observed for the hepta- and octachlorinated compounds. Despite much lower PCDD/PCDF intake after weaning, concentrations in stool fat did not decrease substantially. We conclude that concentrations in fecal fat more or less reflect those in body fat. Additionally, PCDD/PCDF concentrations were measured in blood fat of all infants (and in a second formula-fed baby) at the age of 11 mo. International toxicity equivalent (I-TEq) concentrations in the formula-fed infants were less than 25% of maternal values and about 10 times lower than in the infants breast-fed for 6-7 mo. In the latter, a distinct accumulation was found for the tetra- to hexachlorinated congeners compared with maternal concentrations. We conclude that accumulation of PCDDs and PCDFs in infants is as high as expected on the basis of intake data and assuming complete absorption and negligible elimination during the 1st y of life.

Susceptibility to infections and immune status in Inuit infants exposed to organochlorines.

“…The protection early in life could be related to the transfer of maternal antibodies from the mother to the infant during the first months of breastfeeding. Organochlorines accumulate in the newborn during the breast-feeding period (38)(39)(40) and could eventually reach concentrations that are detrimental to immune system function. However, we could not address the effect of postnatal OC exposure in the present study.…”

Breast milk and lipid intake distributions for assessing cumulative exposure and risk

“…The infant can thus receive a significant portion of toxicants from maternal body stores that have accumulated over decades of exposure (Smith, 1987;Hoover et al, 1991;Schecter et al, 1996). On a bodyweight basis, daily exposure to such contaminants can be markedly greater in breast-fed infants than in adults (Patandin et al, 1999) or formula-fed infants (Abraham et al, 1996). Maternal occupational and pharmaceutical exposures to less persistent (Schreiber et al, 1998) and nonlipophillic substances (e.g., metals; Sonawane, 1995) can also result in significant exposures to nursing infants.…”

Distribution of PCDDs/PCDFs and Co-PCBs in Human Maternal Blood, Cord Blood, Placenta, Milk, and Adipose Tissue: Dioxins Showing High Toxic Equivalency Factor Accumulate in the Placenta

“…Fax: +81-11-386-6040; E-mail: mhnakano@io.ocn.ne.jp Abbreviations: PCDDs, polychlorinated dibenzo-p-dioxins; PCDFs, polychlorinated dibenzofurans; PCBs, polychlorinated biphenyls; Co-PCBs, coplanar PCBs; TeCDD/CDF/CB, tetra CDD/CDF/CB; PeCDD/CDF/CB, penta CDD/CDF/CB; HxCDD/CDF/CB, hexa CDD/CDF/CB; HpCDD/CDF/CB, hepta CDD/CDF/CB; OCDD/CDF/CB, octa CDD/CDF/CB; TEF, toxic equivalency factor; TEQ, toxic equivalency quantity countries, [14][15][16][17][18][19][20][21] but since dioxin levels vary between and within countries, continuous monitoring of dioxin levels in humans is required to gauge exposure.…”