Academic journal article Environmental Health Perspectives

The Association of Prenatal Exposure to Perfluorinated Chemicals with Maternal Essential and Long-Chain Polyunsaturated Fatty Acids during Pregnancy and the Birth Weight of Their Offspring: The Hokkaido Study

Academic journal article Environmental Health Perspectives

The Association of Prenatal Exposure to Perfluorinated Chemicals with Maternal Essential and Long-Chain Polyunsaturated Fatty Acids during Pregnancy and the Birth Weight of Their Offspring: The Hokkaido Study

Article excerpt

Introduction

Perfluorinated chemicals (PFCs) are ubiquitous and stable chemicals widely detected in humans and environment. Contamination of drinking water, house dust, foods, and fish products are the possible major exposure pathways of humans to PFCs (Lau et al. 2007). The most widely studied and detected PFCs are perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA). In 2009, PFOS was added to Annex B of the Stockholm Convention on Persistent Organic Pollutants (POPs) (United Nations Environment Programme 2007). PFOS and PFOA are being voluntarily phased out by several industries, and are being substituted by longer carbon-chain PFCs. Recently, we reported that plasma levels of PFOS and PFOA were generally decreasing in plasma of pregnant Japanese women; however, we observed an increased trend for PFCs with longer carbon chains (Okada et al. 2013). Additionally, PFOS and PFOA are still present in older products, and they are slowly eliminated from the human body, with mean half-lives of 5.4 and 3.8 years for PFOS and PFOA, respectively (Olsen et al. 2007).

Both PFOS and PFOA have been shown to have developmental and reproductive toxicity in animal studies, including early pregnancy loss, reduced fetal weight, and postnatal mortality (Abbott et al. 2007; Luebker et al. 2005). A strong correlation of these compounds has been demonstrated between maternal and cord blood samples in humans, indicating that neonates are exposed to PFCs via the placental passage (Inoue et al. 2004; Monroy et al. 2008). Some epidemiological studies have also reported an association between PFC exposure and poor birth outcomes including decreased birth size (Apelberg et al. 2007; Fei et al. 2007; Washino et al. 2009). In a prospective study, prenatal PFOA exposure was positively associated with the prevalence of overweight female offspring at 20 years of age (Halldorsson et al. 2012). However, Barry et al. (2014) reported no association between early-life PFOA exposure and overweight and obesity risk in adults 20-40 years of age.

Recent research has shown that PFCs perturb metabolic end points, including lipid metabolism, glucose homeostasis, and thyroid hormone balance, in animals (Seacat et al. 2003; Thibodeaux et al. 2003). Such effects might explain associations between PFCs and birth outcomes. Most epidemiological studies regarding the association between PFCs and lipids [triglyceride (TG) and cholesterol] have been conducted in nonpregnant participants. Although previous reports suggest a positive association between PFCs and cholesterol levels (Frisbee et al. 2010; Winquist and Steenland 2014), the reports regarding the association of PFCs and TG levels are inconsistent. In a targeted group of Inuit adults 18-74 years of age, Chateau-Degat et al. (2010) reported a significant negative association between high PFOS exposure levels and TG only in women. However, some groups reported no association between exposure to PFCs and TG levels (Fisher et al. 2013; Sakr et al. 2007) or even a positive association between exposure to PFCs and TG levels in nonpregnant women (Steenland et al. 2009). Therefore, the relevance of these findings is uncertain.

Fetal growth is dependent on maternal metabolic resources, and this is exemplified by the correlation between maternal and fetal TG and fatty acids (FAs) levels (Kitajima et al. 2001; Schaefer-Graf et al. 2011). Major physiologic changes in lipid metabolism take place during normal pregnancies. There is an increase in body fat depots during early pregnancy, whereas lipolysis of fat depots occurs in late pregnancy, resulting in hyperlipidemia. Maternal hyperlipidemia during late pregnancy facilitates the availability of lipid substrates to the fetus. Fetuses need essential fatty acids (EFAs) and long-chain polyunsaturated fatty acids (LCPUFAs) for growth and development, especially for nervous system development (Alvarez et al. 1996). EFAs include linoleic acid and [alpha]-linolenic acid, which are precursors of omega 6 and omega 3 LCPUFAs, respectively. …

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