Higher PFCs when pregnant linked to smaller daughters at birth.
Maisonet, M, ML Terrell, MA McGeehin, KY Christensen, A Holmes, AM Calafat and M Marcus. 2012. Maternal concentrations of polyfluoroalkyl compounds during pregnancy and fetal and postnatal growth in British girls. Environmental Health Perspectives http://dx.doi.org/10.1289/ehp.1003096.
A pregnant woman's exposure to chemicals that make consumer products stain and water resistant may affect the growth and weight of her daughter at birth and later in life as a toddler. A British study has found that newborns whose mothers had higher levels of the polyfluoroalkyl compounds PFOS, PFOA and PFHxS during pregnancy weighed between 3 and 5 ounces less than girls born to mothers with lower levels. At 20 months, the girls born to mothers with higher exposures to PFOS were heavier when compared to those with lower exposures. Prior animal and human studies show similar trends.
Polyfluoroalkyl compounds – usually abbreviated as PFCs – are a group of compounds found in coatings and products that resist heat, oil, stains, grease and water. PFCs can be found in clothing, furniture, fast food packaging, stain-resistant carpeting, electrical wire (CDC) insulation and non-stick products – although cookware is not thought to be a major source of exposure. They also have been used in fire-fighting foams (ATDSR 2009).
PFCs are a concern because they are extremely persistent in the environment, contaminating wildlife and people. Some PFCs may take years to leave the body (Olsen et al. 2007).
Exposure to PFCs is widespread. The main sources are contaminated water and food, but people are also exposed through indoor air and dust (ATDSR 2009; Tittlemier et al. 2007). PFCs have been detected in human serum, cord blood and breast milk.
The most commonly studied PFCs include perfluorooctane sulfonic acid (PFOS), perfluorooctanoic acid (PFOA) and perfluorohexane sulfonate (PFHxS). Chemical companies began phasing out PFOS and PFOA in the last decade with a goal of global elimination by 2015. Yet, consumer products can still have low levels of these PFCs as breakdown products or impurities.
Results from animal and limited human studies suggest that prenatal exposure to PFCs may adversely affect growth before and after birth. In animals, prenatal exposure to PFOS and PFOA has been associated with lower birth weights in the offspring (Hines et al. 2009; Lau et al. 2006; Luebker et al. 2005; Wolf et al. 2007), while prenatal exposure to PFOA has been linked to higher body weights in adult female offspring.
In humans, prenatal exposure to PFOS and PFOA are linked to adverse birth outcomes, such as decreased birth weight, decreased head circumference and reduced birth length (Apelberg et al. 2007; Stein et al. 2009; Washino et al. 2009).
The study examined if pregnant womens' exposure to three PFC compounds affected their daughters' growth before and after birth. Researchers measured concentrations of three PFCs – PFOS, PFOA and PFHxS – in 447 blood samples taken between 1991 and 1992 from pregnant women who lived in the county of Avon, Great Britain. The mother-daughter pairs were participating in the Avon Longitudinal Study of Parents and Children.
Medical records provided fetal growth information, including birth weight, length, gestational age and ponderal index. Health professionals measured the girls' weight and height during routine medical check-ups at approximately 2, 9 and 20 months of age. The women self-reported behavior and lifestyle factors during pregnancy. Breastfeeding information was gathered in questionnaires when the girls were a month old.
Researchers categorized girls into one of three exposure groups based on maternal blood concentrations. They compared fetal and postnatal growth in girls in the middle and highest exposure groups to girls in the lowest exposure group.
In their analysis, researchers considered various factors that could affect the association among the chemicals and prenatal and postnatal growth, including gestational age; the child's breastfeeding history; and the mother's education, pre-pregnancy body mass index, smoking status during pregnancy and race.
All three compounds were detected in every blood sample analyzed.
Median concentrations in blood samples were highest for PFOS (19.6 nanograms per milliliter, ng/mL) followed by PFOA (3.7 ng/mL) and PFHxS (1.6 ng/mL).
For all three, the girls whose mothers were in the highest exposure group weighed less at birth than those born to mothers in the lowest exposure group. On average, girls born to mothers with the highest exposure to PFOS (greater than 23 ng/mL) weighed 4.9 ounces less at birth compared to girls born to mothers in the lowest PFOS exposure group (less than 16.6 ng/mL).
Girls born to mothers in the highest PFOA exposure group (greater than 4.4 ng/mL) weighed about 4.7 ounces less than girls born to mothers in the lowest exposure group (less than 3.1 ng/mL). Girls born to mothers in the highest PFHxS exposure group (more than 2.0 ng/mL) weighed 3.8 ounces less than girls born to mothers in the lowest exposure group (less than 1.3 ng/mL).
High prenatal exposure to PFOS and PFHxS was also associated with decreased birth length.
Additionally, researchers found that by 20 months of age, girls in the highest PFOS exposure group were about 1.3 pounds heavier than girls in the lowest exposure group. Weight changes at 20 months were not observed for PFOA and PFHxS.
A pregnant woman's exposure to chemicals associated with stain and water resistant coatings may influence her daughter's growth and weight at birth and later in life as a toddler.
The findings show that girls whose mothers had higher levels of PFOS, PFOA and PFHxS during pregnancy were 3 to 5 ounces smaller at birth than girls whose mothers had lower exposures. At 20 months, the girls whose mothers had higher exposures to PFOS were heavier when compared to those whose mothers had lower exposures.
Prior studies with animals and people show similar results.
The mothers' blood concentrations for PFOS and PFOA were higher than those reported in previous studies on fetal growth conducted in Japan, Canada and the United States, but lower than those reported in a Danish study (Washino et al. 2009; Hamm et al. 2009; Apelberg et al. 2007; Fei et al. 2008, 2007). In most of these studies, samples were collected after the year 2000. According to the authors, the maternal concentrations of PFCs in this study may be higher because samples were collected in the early 1990’s before some PFCs were voluntarily phased out, so global production rates may have been greater than current rates.
Nonetheless, most of these prior studies also reported associations with PFOS and/or PFOA and adverse effects on fetal growth – decreased birth weight and/or length (Apelberg et al. 2007; Fei et al. 2008, 2007; Washino et al. 2009). A recent study also reported an inverse association with prenatal exposure to PFHxS and birth weight (Lee et al. 2012).
Prenatal exposure to PFOS was associated with increased weight gain at 20 months. It is not known whether the girls in this study continued to gain weight into adulthood. A recent study reported a link between prenatal exposure to PFOA and an increased risk of being overweight or obese in 20-year-old women (Halldorsson et al. 2012). These findings are also in line with one animal study that reported a link between prenatal PFOA exposure and obesity in adulthood (Hines et al. 2009).
Postnatal exposure to the compounds was not assessed, so it is unclear whether exposure during early childhood could have played a role in the observed weight gain. Future studies are needed to see if postnatal exposure to PFCs has similar effects as prenatal exposure.
Apelberg, BJ, FR Witter, JB Herbstman, AM Calafat, RU Halden, LL Needham and LR Goldman. 2007. Cord serum concentrations of perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA)
Fei, C, JK McLaughlin, RE Tarone and J Olsen. 2007. Perfluorinated chemicals and fetal growth: a
Halldorsson, TI, D Rytter, LS Haug, BH Bech, I Danielsen, G Becher, T Brink Henriksen and SF Olsen. 2012. Prenatal exposure to perfluorooctanoate and risk of overweight at 20 years of age: A prospective cohort study. Environmental Health Perspectives 120(5):668-673.
Hamm, MP, NM Cherry, E Chan, JW Martin and I Burstyn. 2010. Maternal exposure to
Hines, EP, SS White, JP Stanko, EA Gibbs-Flournoy, C Lau and SE Fenton. 2009. Phenotypic
Lau, C, JR Thibodeaux, RG Hanson, MG Narotsky, JM Rogers, AB Lindstrom and MJ Strynar. 2006. Effects of perfluorooctanoic acid exposure during pregnancy in the mouse. Toxicological Science 90(2):510-518.
Luebker, DJ, MT Case, RG York, JA Moore, KJ Hansen and JL Butenhoff. 2005. Two-generation
Nolan, LA, JM Nolan, FS Shofer, NV Rodway and EA Emmett. 2009. The relationship between
Olsen, GW, JM Burris, DJ Ehresman, JW Froehlich, AM Seacat, JL Butenhoff and LR Zobel. 2007. Half-life of serum elimination of perfluorooctanesulfonate, perfluorohexanesulfonate, and perfluorooctanoate in retired fluorochemical production workers. Environmental Health Perspectives 115 (9):1298-305.
Tittlemier, SA, K Pepper, C Seymour, J Moisey, R Bronson, XL Cao and RW Dabeka. 2007. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat, fish, fast foods and food items prepared in their packaging. Journal of Agriculture and Food Chemistry 55(8):3203-3210.
Washino, N, Y Saijo, S Sasaki, S Kato, S Ban, K Konishi, R Ito, A Nakata, Y Iwasaki, K Saito, H Nakazawa and R Kishi. 2009. Correlations between
Wolf, CJ, SE Fenton, JE Schmid, AM Calafat, K Kuklenyik, XA Bryant, J Thibodeaux, KP Das,
The above work by Environmental Health News is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License.
Based on a work at www.environmentalhealthnews.org.