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Background: Reported polybrominated diphenyl ether (PBDE) concentrations in human samples in the United States have been higher than in Europe and Asia. Little is known about factors that contribute to individual variability in body burden. Objective: In this large study we measured PBDE concentrations in human milk from the United States during 2004-2006. We assessed characteristics associated with concentrations in milk and change in milk concentration between 3 and 12 months postpartum. Methods: We analyzed 303 milk samples obtained 3 months postpartum for PBDEs. A second sample was analyzed for 83 women still lactating 12 months postpartum. PBDE concentrations in milk and variability by individual characteristics such as age, parity, and prepregnancy body mass index (BMI) were evaluated using generalized linear models. Results: PBDE congeners BDEs 28, 47, 99, 100, and 153 were detected in > 70% of samples. BDE-47 concentrations were the highest, ranging from below the limit of detection to 1,430 ng/g lipid, with a median of 28 ng/g lipid. Concentrations of most individual PBDE congeners and the sum of BDEs 28, 47, 99, 100, and 153 (ΣPBDE) were lower among mothers > 34 years of age compared with those 25-29 years of age and higher among mothers with high compared with normal BMI, after adjustment for other covariates. Parity was not associated with PBDE concentration. The change in ΣPBDE concentration in milk between 3 and 12 months postpartum was highly variable (median increase, 14%; interquartile range, -26% to 50%). Conclusions: PBDEs were detected in nearly all human milk samples, varying by maternal weight and age and over the course of breast-feeding. [ABSTRACT FROM AUTHOR]

Background: In many parts of the world, deliberate indoor residual spraying (IRS) of dwellings with insecticides to control malaria transmission remains the only viable option, thereby unintentionally but inevitably also causing exposure to inhabitants. Because mothers are exposed to insecticides via various routes, accumulated residues are transferred to infants via breast milk, in some cases exceeding recommended intake levels. Except for dichlorodiphenyltrichloroethane (DDT), safety of residues of other insecticides in breast milk has not been considered during World Health Organization Pesticide Evaluation Scheme (WHOPES) evaluations. However, very little is known of the health risks posed by these chemicals to infants who, in developing countries, breast-feed for up to 2 years. Objective: We evaluated the need for WHOPES to include breast milk as a potentially significant route of exposure and risk to infants when evaluating the risks during evaluation of IRS insecticides. Discussion: We present evidence showing that neurologic and endocrine effects are associated with pyrethroids and DDT at levels equal or below known levels in breast milk. Conclusions: Because millions of people in malaria control areas experience conditions of multiple sources and routes of exposure to any number of insecticides, even though lives are saved through malaria prevention, identification of potential infant health risks associated with insecticide residues in breast milk must be incorporated in WHOPES evaluations and in the development of appropriate risk assessment tools. [ABSTRACT FROM AUTHOR]

BACKGROUND: Polychlorinated biphenyls (PCBs) and dichlorodiphenyltrichloroethane (DDT) are persistent, bioaccumulative, and toxic pollutants that were broadly used in the United States until the 1970s. Common exposure to PCBs, DDT, and dichlorodiphenyldichloroethylene (DDE), the most stable metabolite of DDT, may influence children's neurodevelopment, but study results are not consistent. OBJECTIVES: We examined the associations between lactational exposure to PCBs, DDT, and DDE and infant development at 12 months, using data from the Pregnancy, Infection, and Nutrition Babies Study, 2004--2006. METHODS: We measured PCBs, DDT, and DDE in breast milk at the third month postpartum. Lactational exposure of these chemicals was estimated by the product of chemical concentrations and the duration of breast-feeding. Infant development at 12 months of age was measured by the Mullen Scales of Early Learning (n = 231) and the Short Form: Level I (infant) of the MacArthur--Bates Communicative Development Indices (n = 218). RESULTS: No consistent associations were observed between lactational exposure to PCBs, DDT, and DDE through the first 12 months and the measures of infant development. However, DDE was associated with scoring below average on the gross motor scale of the Mullen among males only (adjusted odds ratio = 1.9; 95% confidence interval, 1.1--3.3). CONCLUSION: Infant neurodevelopment at 12 months of age was not impaired by PCBs, DDT, and DDE at the concentrations measured here, in combination with benefits from long duration of breast-feeding in this population. [ABSTRACT FROM AUTHOR]

BACKGROUND: One of the most serious human health concerns related to environmental contamination with polychlorinated biphenyls (PCBs) is the presence of these chemicals in breast milk. OBJECTIVES: We developed a physiologically based pharmacokinetic model of PCB-153 in women, and predict its transfer via lactation to infants. The model is the first human, population-scale lactational model for PCB-153. Data in the literature provided estimates for model development and for performance assessment. METHODS: We used physiologic parameters from a cohort in Taiwan and reference values given in the literature to estimate partition coefficients based on chemical structure and the lipid content in various body tissues. Using exposure data from Japan, we predicted acquired body burden of PCB-153 at an average childbearing age of 25 years and compared predictions to measurements from studies in multiple countries. We attempted one example of reverse dosimetry modeling using our PBPK model for possible exposure scenarios in Canadian Inuits, the population with the highest breast milk PCB-153 level in the world. RESULTS: Forward-model predictions agree well with human biomonitoring measurements, as represented by summary statistics and uncertainty estimates. CONCLUSION: The model successfully describes the range of possible PCB-153 dispositions in maternal milk, suggesting a promising option for back-estimating doses for various populations. [ABSTRACT FROM AUTHOR]

The article discusses the risks and benefits of breastfeeding and the dangers that contaminants such as heavy metals in human milk pose to newborns. Topics include a brief biological history of breastfeeding, the socio-cultural changes throughout the 1800 and 1900s, and statistics related to breastfeeding mothers in the U.S. and developing countries. Also discussed are the immunological benefits of breast milk, such as defense against pathogens and inflammation, the effect of persistent organic pollutants (POPs) such as polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and polychlorinated biphenyls (PCBs) on infant development, and the World Health Organization's (WHO) stance on breastfeeding.

BACKGROUND: Chronic arsenic exposure causes a wide range of health effects, but little is known about critical windows of exposure. Arsenic readily crosses the placenta, but the few available data on postnatal exposure to arsenic via breast milk are not conclusive. AIM: Our goal was to assess the arsenic exposure through breast milk in Bangladeshi infants, living in an area with high prevalence of arsenic-rich tube-well water. METHODS: We analyzed metabolites of inorganic arsenic in breast milk and infant urine at 3 months of age and compared them with detailed information on breast-feeding practices and maternal arsenic exposure, as measured by concentrations in blood, urine, and saliva. RESULTS: Arsenic concentrations in breast-milk samples were low (median, 1 µg/kg; range, 0.25--19 µg/kg), despite high arsenic exposures via drinking water (10--1,100 µg/L in urine and 2--40 µg/L in red blood cells). Accordingly, the arsenic concentrations in urine of infants whose mothers reported exclusive breast-feeding were low (median, 1.1 µg/L; range, 0.3--29 µg/L), whereas concentrations for those whose mothers reported partial breast-feeding ranged from 0.4 to 1,520 µg/L (median 1.9 µg/L). The major part of arsenic in milk was inorganic. Still, the infants had a high fraction (median, 87%) of the dimethylated arsenic metabolite in urine. Arsenic in breast milk was associated with arsenic in maternal blood, urine, and saliva. CONCLUSION: Very little arsenic is excreted in breast milk, even in women with high exposure from drinking water. Thus, exclusive breast-feeding protects the infant from exposure to arsenic. [ABSTRACT FROM AUTHOR]

BACKGROUND: Polybrominated diphenyl ethers (PBDEs) are capable of disrupting thyroid hormone homeostasis. PBDE-47 (2,2',4,4'-tetrabromodiphenyl ether) is one of the most abundant congeners found in human breast adipose tissue and maternal milk samples. OBJECTIVES: We evaluated the effects of developmental exposure to low doses of PBDE-47 on the female reproductive system. METHODS: Pregnant Wistar rats were administered vehicle (peanut oil) or PBDE-47 [140 or 700 μg/kg body weight (bw)] on gestation day (GD) 6, or 5 mg 6-n-propyl-2-thiouracil (PTU)/L in the drinking water from GD7 through postnatal day (PND) 21. RESULTS: In female offspring sacrificed on PND38, there was a significant decrease in ovarian weight after exposure to PTU or 140 μg/kg PBDE-47. Alterations in folliculogenesis were apparent: we observed a decrease in tertiary follicles and serum estradiol concentrations in the offspring exposed to either PTU or 700 μg/kg PBDE-47. PTU exposure also resulted in a decrease in primordial follicles. On PND100, persistent effects on the thyroid glands included histologic and morphometric changes after exposure to either PTU or PBDE-47. No relevant changes in reproductive indices were observed after mating the exposed F1 females with nontreated males. CONCLUSIONS: Administration of PBDE-47 at doses relevant to human exposure led to changes in the rat female reproductive system and thyroid gland. [ABSTRACT FROM AUTHOR]

Phthalates adversely affect the male reproductive system in animals. We investigated whether phthalate monoester contamination of human breast milk had any influence on the postnatal surge of reproductive hormones in newborn boys as a sign of testicular dysgenesis. Design: We obtained biologic samples from a prospective Danish-Finnish cohort study on cryptorchidism from 1997 to 2001. We analyzed individual breast milk samples collected as additive aliquots 1-3 months postnatally (n = 130; 62 cryptorchid/68 healthy boys) for phthalate monoesters [mono-methyl phthalate (mMP), mono-ethyl phthalate (mEP), mono-n-butyl phthalate (mBP), mono-benzyl phthalate (mBzP), mono-2-ethylhexyl phthalate (mEHP), mono-isononyl phthalate (miNP)]. We analyzed serum samples (obtained in 74% of all boys) for gonadotropins, sex-hormone binding globulin (SHBG), testosterone, and inhibin B. Results: All phthalate monoesters were found in breast milk with large variations [medians (minimum-maximum)]: mMP 0.10 (< 0.01-5.53 µg/L), mEP 0.95 (0.07-41.4 µg/L), mBP 9.6 (0.6-10,900 µg/L), mBzP 1.2 (0.2-26 µg/L), mEHP 11 (1.5-1,410 µg/L), miNP 95 (27-469 µg/L). Finnish breast milk had higher concentrations of mBP, mBzP, mEHP, and Danish breast milk had higher values for miNP (p = 0.0001-0.056). No association was found between phthalate monoester levels and cryptorchidism. However, mEP and mBP showed positive correlations with SHBG (r = 0.323, p = 0.002 and r = 0.272, p = 0.01, respectively); mMP, mEP, and mBP with LH:free testosterone ratio (r = 0.21-0.323, p = 0.002-0.044) and miNP with luteinizing hormone (r = 0.243, p = 0.019). mBP was negatively correlated with free testosterone (r = -0.22, p = 0.033). Other phthalate monoesters showed similar but nonsignificant tendencies. Conclusions: Our data on reproductive hormone profiles and phthalate exposures in newborn boys are in accordance with rodent data and suggest that human Leydig cell development and function may also be vulnerable to perinatal exposure to some phthalates. Our findings are also in line with other recent human data showing incomplete virilization in infant boys exposed to phthalates prenatally.

Increasing concentrations of polybrominated flame retardants, including polybrominated diphenyl ethers (PBDEs), in breast milk cause concern about possible developmental effects in nursed babies. Because previous studies in rats have indicated effects on sex steroids and sexually dimorphic behavior after maternal exposure to polychlorinated biphenyls (PCBs), our goal in the present study was to determine if developmental exposure to 2,2´,4,4´,5-pentabromodiphenyl ether (PBDE-99) induces similar endocrine-mediated effects. Pregnant rats were exposed to vehicle or PBDE-99 (1 or 10 mg/kg body weight, daily during gestational days 10-18). For comparison, we also included a group exposed to the technical PCB mixture Aroclor 1254 (30 mg/kg body weight, daily). PBDE exposure resulted in pronounced decreases in circulating sex steroids in male offspring at weaning and in adulthood. Female offspring were less affected. Anogenital distance was reduced in male offspring. Puberty onset was delayed in female offspring at the higher dose level, whereas a slight acceleration was detected in low-dose males. The number of primordial/primary ovarian follicles was reduced in females at the lower dose, whereas decline of secondary follicles was more pronounced at the higher dose. Sweet preference was dose-dependently increased in PBDE-exposed adult males, indicating a feminization of this sexually dimorphic behavior. Aroclor 1254 did not alter sweet preference and numbers of primordial/primary and secondary follicles but it did affect steroid concentrations in males and sexual development in both sexes. PBDE concentrations in tissues of dams and offspring were highest on gestational day 19. These results support the hypothesis that PBDEs are endocrine-active compounds and interfere with sexual development and sexually dimorphic behavior. [ABSTRACT FROM AUTHOR]

Nursing infants may be exposed to lead from breast milk, but relatively kw data exist with which to evaluate and quantify this relationship. This route of exposure constitutes a potential infant hazard from mothers with current ongoing exposure to lead as well as from mothers who have been exposed previously due to the redistribution of cumulative maternal bone lead stores. We studied the relationship between maternal breast milk lead and infant blood lead levels among 255 mother-infant pairs exclusively or partially breast-feeding through I month of age in Mexico City. A rigorous, well-validated technique was used to collect, prepare, and analyze the samples of breast milk to minimize the potential for environmental contamination and maximize the percent recovery of lead. Umbilical cord and maternal blood lead were measured at delivery; I month after delivery (± 5 days) maternal blood, bone, and breast milk and infant blood lead levels were obtained. Levels of lead at I month postpartum were, for breast milk, 0.3-8.0 μg/dL (mean ± SD, 1.5 ± 1.2); maternal blood lead, 2.9-29.9 μg/dL (mean ± SD, 9.4 ± 4.5); and infant blood lead, 1.0-23.1 μg/dL (mean ± SD, 5.5 ± 3.0). Infant blood lead at I month postpartum was significantly correlated with umbilical cord (Spearman correlation coefficient rs = 0.40, p < 0.0001) and maternal (rs = 0.42, p < 0.000 1) blood lead at delivery and with maternal blood (rs = 0.67, p <0.0001), patella (rs= 0.I9,p = 0.004), and breast milk (rs= 0.32,p < 0.0001) lead at I month postpartum. Adjusting kr cord blood lead, infant weight change, and reported breast-feeding status, a difference of approximately 2 μg/dL (ppb; from the midpoint of the lowest quartile to the midpoint of the highest quartile) breast milk lead was associated with a 0.82 μg/dL increase in blood lead for breast-feeding infants at I month of age. Breast milk lead accounted for 12% of the variance of infant blood lead levels, whereas maternal blood lead accounted kr 30%. Although these levels of lead in breast milk were low, they clearly have a strong influence on infant blood lead levels over and above the influence of maternal blood lead. Additional information on the lead content of dietary alternatives and interactions with other nutritional factors should be considered. However, because human milk is the best and most complete nutritional source for young infants, breast-feeding should be encouraged because the absolute values of the effects are small within this range of lead concentrations. Key words: blood lead, breast milk lead, breast-feeding, [ABSTRACT FROM AUTHOR]

Polybrominated diphenyl ether (PBDE) congeners are constituents of flame retardants, and there is growing concern regarding their persistence, bioaccumulation, and toxicity. We collected breast milk samples between late 2001 and early 2003 from 54 U.K.-resident mothers. Of these, 27 originated from southeast England (London), and the other 27 originated from northwest England (Lancaster). Analysis of milk-fat extracts by gas chromatography-mass spectrometry was performed to determine the levels of 15 PBDE congeners, 15 polychlodnated biphenyl (PCB) congeners, and other selected chlorinated compounds. PCB and organochlorine (OC) levels in southeast samples were consistently higher, and significant differences (p < 0.05) were observed. ∑PBDE levels ranged from 0.3 to 69 ng/g lipid (geometric mean, 6.6 ng/g), and PBDE47 was the most abundant congener. ∑PCB levels ranged from 26 to 530 ng/g lipid (geometric mean, 150 ng/g) and were composed mainly of PCB-153 (26%), PCB-138 (20%), and PCB-180 (13%). OC levels for 1,1,1-trichloro-2,2bis(p-chlorophenyt)ethane (p,p'-DDT) and its metabolites (∑DDX) ranged from 24 to 2,300 ng/g lipid (geometric mean, 160 ng/g); hexachlorobenzene ranged from nondetectable levels to 180 ng/g lipid (geometric mean, 17 ng/g); and ∑hexachlorocydohexane levels ranged from 1.2 to 1,500 ng/g lipid (geometric mean, 16 ng/g). Using nuclear magnetic resonance-based metabonomics, samples (n = 7) containing the highest contaminant levels were compared with samples (n = 7) containing the lowest levels. Excellent separation along the first principal component implied that the chemical constituents of the two groups were significantly different. Although reasons for such differences remain obscure, lifestyle factors associated with a more heterogeneous London cohort could be responsible. Identifying primary routes of contaminant exposures and their biologic effects is of great importance. . . [ABSTRACT FROM AUTHOR]

Examines the patterns of chemical contaminants in breast milk. Decline in the levels of organochlorine pesticides, polychlorinated biphenyls and dioxins; Increase in the levels of polybrominated diphenyl ethers; Role of diet in breast milk levels of organic pollutants.

Examines the pharmacokinetics of toxic chemicals in breast milk in the U.S. Use of physiologically based pharmacokinetic models to predict infant exposure via breast milk; Benefits of the quantitative models; Incorporation of time-dependent changes in physiologic characteristics on the model.

Examines the infant body burden of dioxin-like compounds from breast-feeding using first-order pharmacokinetic model. Importance of the assumption of the rate of dissipation of toxic equivalents in breast-fed infants; Evaluation of nursing scenarios; Decline in dioxin concentration.

Examines the presence of environmental chemicals in human breast milk. Health consequence of the chemical to the breast-fed infants and the mother; List of environmental chemicals found in breast milk; Approaches in measuring environmental chemicals.

Examines the geographic distribution of selenium concentration in breast milk samples in Poland. Regions with the highest and the lowest selenium concentrations; Determination of whether the cause of the concentration is natural or environmental.

Reports on the levels of polybrominated diphenyl ethers (PBDE) in human breast milk and the relevance of breast milk monitoring programs. Usage, occurrence and toxicity of PBDE; Parallels between PBDE and other polyhalogenated persistent organic pollutants; Future environmental challenges posed by PBDE.

The article discusses various reports published within the issue, including one about contaminants in breast milk, one about children encountering nature, and one about lead exposure in U.S. children.

Examines the infectious and chemical hazards in breast milk. Activities undertaken by World Health Organization on breast milk contamination; Comparison between artificial feeding and breast feeding; Need to control the use of toxic products.

Examines the chemical contaminants in breast milk in the U.S. Impact of toxic chemicals on the health of infants; Insufficiency of information on the nature and levels of contaminants in breast milk; Absence of consistent protocol for collecting and analyzing breast milk samples.

The article discusses the potential health risks of xenobiotic exposures to breastfed infants through human milk. A pharmacokinetic model of polychlorinated biphenyl (PCB)-153 was developed to predict the transfer of PCB-153 through breastfeeding. The model's predictions fell within ranges reported in previous studies. The implications of the model are also discussed.

The article reports on a study in Bangladesh concerning breastfed infants' exposure to arsenic. Participants in the Maternal and Infant Nutrition Interventions program were tested for arsenic metabolites and breast milk samples were analyzed. Researchers found that the breast milk contained an inorganic arsenite form which can protect infants.

Investigates the exposure and health effects in children whose mothers were exposed to dioxins and polychlorinated biphenyls (PCB) in The Netherlands. Exposure of children through breast milk; Development effects on neurobehavioral, hormonal and immunological areas; Decrease in circulating neuro-optimality and circulating thyroxine levels.