Relationship of Perfluorooctanoic Acid Exposure to Pregnancy Outcome Based on Birth Records in the Mid-Ohio Valley

Abstract

Background: Perfluorooctanoic acid (PFOA) is a potential cause of adverse pregnancy outcomes, but previous studies have been limited by low exposures and small study size.Objectives: Using birth certificate information, we examined the relation between estimated PFOA exposure and birth outcomes in an area of West Virginia and Ohio whose drinking water was contaminated by a chemical plant.Methods: Births in the study area from 1990 through 2004 were examined to generate case groups of stillbirth (n = 106), pregnancy-induced hypertension (n = 224), preterm birth (n = 3,613), term low birth weight (n = 918), term small-for-gestational-age (SGA) (n = 353), and a continuous measure of birth weight among a sample of term births (n = 4,534). A 10% sample of term births ≥ 2,500 g were selected as a source of controls (n = 3,616). Historical estimates of serum PFOA were derived from a previously developed fate and transport model. In a second study, we examined 4,547 area births linked to a survey with residential history data.Results: In the analysis based only on birth records, we found no consistent evidence of an association between estimated PFOA exposure and stillbirth, pregnancy-induced hypertension, preterm birth, or indices of fetal growth. In the analysis of birth records linked to the survey, PFOA was unrelated to pregnancy-induced hypertension or preterm birth but showed some suggestion of an association with early preterm birth. Measures of growth restriction showed weak and inconsistent associations with PFOA.Conclusions: Based on the analysis using the health survey, these results provide little support for an effect of PFOA exposure on most pregnancy outcomes, except for early preterm birth and possibly fetal growth restriction.

Per- and polyfluorinated substances (PFASs): Environmental challenges

“…No association was seen between elevated PFOA exposure and pregnancy outcomes, including miscarriage, stillbirth or birth defects, lowered birth weight [288,289], but for some suggestion of early preterm birth and possibly fetal growth restriction [290]. No association of PFOA with birth defects was found but further investigation was recommended for the brain [291].…”

“…No association of PFOA with birth defects was found but further investigation was recommended for the brain [291]. A weak association of PFOA and PFOS for pregnancy-induced hypertension and preeclampsia was noted [289,290,292,293]. A modest negative association of PFOS serum level with birth weight was reported [293].…”

Biomarker-Based Calibration of Retrospective Exposure Predictions of Perfluorooctanoic Acid

“…20,21 The first model was selected for its simplicity and identifiability with only one serum measurement per participant. The second model was designed to emphasize the temporal relationship between historical PFOA exposures and 2005–2006 serum PFOA concentrations.…”

Per- and polyfluorinated substances in the Nordic Countries

“…The following associations have been seen for PFOA in the "C8 Health Project": increased total cholesterol and low-density lipoprotein in children and adolescents (Frisbee et al, 2010); increased blood lipid levels in relation to elevated PFOA (and PFOS) concentrations in the blood ; no associations to HDL cholesterol; positive associations with serum and liver enzymes (transaminase; a marker of hepatocellular damage) indicating hepatotoxic effect in humans (Gallo et al, 2012); positive association to serum uric acid (Steenland et al, 2010); no association between PFOA and TSH (n = 371) (Emmett et al, 2006); significant positive elevation in serum T4 and a significant reduction in T3 uptake in adults (Knox et al, 2011a); no associations with preterm birth and fetal growth restrictions (Savitz et al, 2012), positive association with hypothyroidism in children (Odds ratio (OR): 1.54; 95% confidence interval (CI): 1.00, 2.37) ; associations with Attention Deficit Hyperactivity Disorder (ADHD) in children 5-18 years of age, with a small increase in prevalence for the second quartile of exposure and a decrease for the highest versus lowest quartile (Stein and Savitz, 2011); more likely to have experienced menopause among perimenopausal women with higher level of PFOA (and PFOS), suggesting endocrine disrupting effects (Knox et al, 2011b); association with lower serum concentrations of IgA and IgE (for IgE in females only) (C8 Science Panel, 2009).…”