Maternal Perfluorooctane Sulfonate Research Articles

Maternal concentrations of perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) and duration of breastfeeding

Perfluorooctanoate (PFOA) has been associated with impaired lactation in mice. We examined whether maternal perfluorooctanesulfonate (PFOS) and PFOA concentrations correlated with duration of breastfeeding among women. We randomly selected 1400 pregnant women from the Danish national birth cohort (1996-2002) and measured PFOS and PFOA concentrations in early pregnancy by using high performance liquid chromatography/tandem mass spectrometry. Self-reported data on the duration of any and exclusive breastfeeding were collected twice during telephone interviews around 6 and 18 months after the birth of the child. The duration of breastfeeding decreased with increasing concentrations of pregnancy PFOS and PFOA among multiparous women, for whom the adjusted odds ratios (OR) for weaning before 6 months of age were 1.20 (95% CI 1.06-1.37) per 10 ng/ml increase in PFOS concentrations and 1.23 (95% CI 1.13-1.33) per 1 ng/ml increase in PFOA concentrations. No consistent association was found for primiparous women. These findings suggest that PFOA and PFOS may reduce the ability to lactate, but could equally reflect reverse causation since no association was seen in primiparous women.

Perfluorinated compounds in maternal serum and cord blood from selected areas of South Africa: results of a pilot study

There is limited information about both environmental and human perfluorinated compounds (PFCs) concentrations in the southern hemisphere, and for the first time, concentrations of these compounds are reported in maternal serum and cord blood of South African women. The majority of the participants were of African Black ethnicity, with a similar socioeconomic status. In maternal serum perfluorooctane sulfonate (PFOS) was found to be the most abundant PFC (1.6 ng mL(-1)), followed by perfluorooctanoate (PFOA: 1.3 ng mL(-1)) and perfluorohexane sulfonate (PFHxS: 0.5 ng mL(-1)); however, in cord blood PFOA was the most abundant compound (1.3 ng mL(-1)) followed by PFOS (0.7 ng mL(-1)) and PFHxS (0.3 ng mL(-1)). Linear PFOS constituted 58% of the sum of PFOS, comparable with a reported percentage from Australia. Differences in PFC concentrations between communities were found, with the highest concentrations in urban and semi-urban areas. The median maternal PFOS concentration was lower than has been reported in other studies, whereas the PFOA concentration was the same. This clearly indicates that the exposure pathway is different from the western world. Significant differences in housing quality were observed and the urban and sub-urban community had the highest living and housing standards. Possible exposure pathways could be different from those elucidated in the western world with the exception of the urban community in our study that showed higher living standards in general and easier access to modern consumer products.

Combined effects of perfluorooctane sulfonate (PFOS) and maternal restraint stress on hypothalamus adrenal axis (HPA) function in the offspring of mice

Although it is known that prenatal exposure to perfluorooctane sulfonate (PFOS) can cause developmental adverse effects in mammals, the disruptive effects of this compound on hormonal systems are still controversial. Information concerning the effects of PFOS on hypothalamus adrenal (HPA) axis response to stress and corticosterone levels is not currently available. On the other hand, it is well established that stress can enhance the developmental toxicity of some chemicals. In the present study, we assessed the combined effects of maternal restraint stress and PFOS on HPA axis function in the offspring of mice. Twenty plug-positive female mice were divided in two groups. Animals were given by gavage 0 and 6 mg PFOS/kg/day on gestation days 12–18. One half of the animals in each group were also subjected to restraint stress (30 min/session, 3 sessions/day) during the same period. Five plug-positive females were also included as non-manipulated controls. At 3 months of age, activity in an open-field and the stress response were evaluated in male and female mice by exposing them to 30 min of restraint stress. Male and female offspring were subsequently sacrificed and blood samples were collected to measure changes in corticosterone levels at four different moments related to stress exposure conditions: before stress exposure, immediately after 30 min of stress exposure, and recuperation levels at 60 and 90 min after stress exposure. Results indicate corticosterone levels were lower in mice prenatally exposed to restraint. In general terms, PFOS exposure decreased corticosterone levels, although this effect was only significant in females. The recuperation pattern of corticosterone was mainly affected by prenatal stress. Interactive effects between PFOS and maternal stress were sex dependent. The current results suggest that prenatal PFOS exposure induced long-lasting effects in mice.

Perfluoroalkyl chemicals and human fetal development: An epidemiologic review with clinical and toxicological perspectives

Epidemiologists began to focus on human developmental outcomes with perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) as a consequence of dose-dependent developmental toxicological studies that reported effects of lowered birth weight, increased postnatal mortality, and decreased postnatal growth in surviving rats and mice. Contributing to the epidemiologic interest was the widespread presence of PFOS and PFOA in the general population, lengthy serum elimination half-lives in humans, and the placental transfer of PFOS and PFOA in humans that was established via measurement of paired maternal and umbilical cord blood samples. The purpose of this paper is to qualitatively review the published epidemiologic literature as it pertains to the potential association of exposure to PFOS and PFOA with human fetal development. The published research has focused on birth weight and other measurements that reflect human fetal development. A total of eight epidemiologic studies were reviewed that focused on six general (non-occupational) and two occupational populations. Of the six general population studies, five examined associations between birth weight and other anthropometric measurements in relation to maternal blood and/or umbilical cord concentrations of PFOS and PFOA. In the sixth study, three geographical areas in Washington County, Ohio, were categorized by their public drinking water sources that contained PFOA that had resulted in higher serum concentrations than observed in other general population studies. The occupational studies focused on a perfluorochemical manufacturing site (Decatur, AL) with exposure categorized from work history and biomonitoring data. There were inconsistent associations reported for several different birth outcomes, including birth weight, birth length, head circumference, and ponderal index, among the five general population studies that measured PFOS and PFOA in the study subjects. No association with birth weight or gestational age was reported in the community drinking water study. Only one general population study examined infant Apgar scores and developmental milestones at 6 and 18 months of age with no associations reported. No association with self-reported birth weight and occupational exposure to PFOS materials was observed among female perfluorochemical production workers. These epidemiologic data are discussed in relation to their methodological strengths and weaknesses, coherence with toxicological results, consistency of associations between studies, and plausible alternative explanations. Epidemiological, clinical, and toxicological insights are offered that may be useful for human health risk characterization. Studies scheduled for completion in the next few years are also cited. An appendix to this review describes the results of the only investigation that attempted to determine whether a causal association existed between maternal (4–14 weeks gestation) PFOS and PFOA concentrations in a general population and fecundity, as measured by time to pregnancy (TTP). Important issues are addressed regarding the methods and data analysis that may limit inferences from this particular study.

Developing Story: No Link Observed between Prenatal PFOA/PFOS Exposure and Milestone Achievement

Vol. 116, No. 10 EnvironewsOpen AccessDeveloping Story: No Link Observed between Prenatal PFOA/PFOS Exposure and Milestone Achievement Valerie J. Brown Valerie J. Brown Search for more papers by this author Published:1 October 2008https://doi.org/10.1289/ehp.116-a441aAboutSectionsPDF ToolsDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InRedditEmail Perfluorooctanoate (PFOA; also known as perfluorooctanoic acid) and perfluorooctanesulfonate (PFOS), chemicals used in waterproofing fabrics and greaseproofing fast-food containers, among other applications, have been detected at low concentrations in 98% of the U.S. population. These chemicals have half-lives of several years, and children tend to have higher serum concentrations than adults. Animal and human studies have hinted at a link between PFOA and PFOS and developmental effects, but human studies have been limited. A new human study suggests that maternal plasma levels of PFOA and PFOS may not be associated with delayed early development in babies [EHP 116:1391–1395; Fei et al.].The research team randomly selected 1,400 mother–baby pairs from the Danish National Birth Cohort comprising 100,000 women recruited during early pregnancy between 1996 and 2002. The team measured PFOA and PFOS levels in maternal blood samples taken in the first trimester of pregnancy. Each newborn’s Apgar score was obtained from Danish hospital records; this assessment of viability taken immediately after birth measures heart rate, respiratory effort, reflex irritability, muscle tone, and skin color.When the children were 6 and 18 months old, their mothers provided data on gross and fine motor functioning, attention, cognitive function, language, and social-personal development via computer-assisted telephone interviews. The study was funded by the International Epidemiology Institute, which received money from the 3M Company, the original manufacturer of PFOA and PFOS, and the 3M Toxicology Laboratory performed the chemical analyses.Earlier human and animal studies suggested that PFOA and PFOS might reduce fetal growth, delay learning, accelerate or delay sexual maturation, and produce other developmental effects. The current study found no significant association between maternal PFOA/PFOS levels and child achievement of early developmental milestones such as walking without support, taking off socks and shoes when asked, and turning a picture book right side up. However, a statistically nonsignificant association was observed between higher maternal PFOS levels and delay of a child’s ability to sit without support.PFOA and PFOS were significantly higher among first-time mothers than in women who had given birth previously. This may confound their results, because the presence of older siblings may accelerate the developmental progress of younger ones. Given animal studies showing potential adverse effects of PFOA and PFOS, and the limited data for humans, the authors write that additional studies should be conducted using more sensitive measures of early childhood development.FiguresReferencesRelatedDetails Vol. 116, No. 10 October 2008Metrics About Article Metrics Publication History Originally published1 October 2008Published in print1 October 2008 Financial disclosuresPDF download License information EHP is an open-access journal published with support from the National Institute of Environmental Health Sciences, National Institutes of Health. All content is public domain unless otherwise noted. Note to readers with disabilities EHP strives to ensure that all journal content is accessible to all readers. However, some figures and Supplemental Material published in EHP articles may not conform to 508 standards due to the complexity of the information being presented. If you need assistance accessing journal content, please contact ehponline@niehs.nih.gov. Our staff will work with you to assess and meet your accessibility needs within 3 working days.

Fetal Growth Indicators and Perfluorinated Chemicals: A Study in the Danish National Birth Cohort

Perfluorooctanoate (PFOA) and perfluorooctanesulfonate (PFOS) are widespread persistent organic pollutants that have been associated with reduced birth weight at doses expected in many pregnant populations. The authors randomly selected 1,400 pregnant women and their newborns from the Danish National Birth Cohort (1996-2002) to investigate whether these compounds reduce organ growth. PFOS and PFOA were measured in maternal blood samples taken early in pregnancy. Placental weight, birth length, and head and abdominal circumferences were measured shortly after birth by trained midwives or nurses. Maternal PFOA levels in early pregnancy were associated with smaller abdominal circumference and birth length. For each ng/ml increase in PFOA, birth length decreased by 0.069 cm (95% confidence interval: 0.024, 0.113) and abdominal circumference decreased by 0.059 cm (95% confidence interval: 0.012, 0.106). An inverse association was also observed between PFOA and placental weight and head circumference, and a positive association was observed with newborn ponderal index, but none of these associations was statistically significant. Maternal PFOS levels were not associated with any of the five fetal growth indicators. These findings suggest that fetal exposure to PFOA but not PFOS during organ development may affect the growth of organs and the skeleton.

Gestational Exposure to Perfluorooctane Sulfonate Suppresses Immune Function in B6C3F1 Mice

Perfluorinated alkyl acids (PFAAs) are used in a multitude of applications and are categorized as high-production volume chemicals produced in quantities exceeding 10,000 lbs/year. As a result, widespread exposure has been documented in adults, children, and infants. It is generally accepted that children are more sensitive to the effects of xenobiotic exposures during fetal and postnatal periods of development; therefore, considerable efforts are required to investigate the potential impact of a model PFAA, perfluorooctane sulfonate (PFOS) on children's immunological health. Using the pairing of female C57BL/6N mice with male C3H/HeJ, developmental immunotoxicity was evaluated in B6C3F1 pups following oral maternal exposure to PFOS on gestations days 1-17. Exposure levels included 0.1, 1, and 5 mg/kg/day PFOS. Natural killer (NK) cell activity, SRBC IgM plaque assay, CD4/8 lymphocytic subpopulations, nitrite production in peritoneal macrophages, and body/organ weights were evaluated at 4 and 8 weeks of age in F1 pups. No significant dose-responsive changes in maternal or pup body weights, flow cytometry, or macrophage function were observed, yet hepatomegaly was indicated in F1 male pups at 4 weeks of age. Functional deficits were not evident until 8 weeks of age when NK cell function and IgM production were significantly decreased. When compared with females, male pups were more sensitive to the effects of PFOS thereby establishing a no observed adverse effect level and low observed adverse effect level of 0.1 and 1.0 mg/kg/day (males only) following maternal PFOS exposure level, respectively. This study establishes that the developing immune system is sensitive to the effects of PFOS and results in functional deficits in innate and humoral immunity detectable at adulthood.

Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat.

The critical period for increased neonatal mortality induced by perfluorooctane sulfonate (PFOS) exposure was evaluated in the rat. Timed-pregnant Sprague-Dawley rats were treated by oral gavage with 25 mg/kg/d PFOS/K(+) on four consecutive days (gestation days (GD) 2-5, 6-9, 10-13, 14-17, or 17-20) or with 0, 25, or 50 mg/kg/d PFOS/K(+) on GD 19-20. Controls received vehicle (10 ml/kg 0.5% Tween-20) on these days. Maternal weight gain was reduced in treated animals during dosing, as were food and water consumption. Following a 4-day treatment, litter size at birth was unaffected while pup weight was similarly reduced in the three earliest PFOS groups. All PFOS groups experienced decreases in survival while controls remained near 100%. Neonatal survival decreased in groups dosed later during gestation, approaching 100% with dosing on GD 17-20. Most deaths occurred before postnatal day (PND) 4, with the majority in the first 24 hours. Maternal serum PFOS levels on GD 21 were higher in groups exhibiting higher mortality. Following a 2-day treatment, PFOS groups experienced significant pup mortality by PND 1. Neonatal mortality continued through PND 5, when survival was 98, 66, and 3% for the 0, 25, and 50 mg/kg groups, respectively. Pup weight was reduced in treated groups with surviving litters. Gross dissection and histological examination of lungs revealed differences in maturation between control and treated animals on PND 0. We conclude that exposure to PFOS late in gestation is sufficient to induce 100% pup mortality and that inhibition of lung maturation may be involved.