The Wall Street Journal Reported yesterday "No Ill Effect Found in Human BPA Exposure" by R. L. Hotz Feb 6-17 2013 p. A3.
"Human exposure to a controversial ingredient in many plastic bottles and food containers is too low to be worrisome, according to a closer look at 150 studies of an additive called bisphenol A, widely known as BPA."
Majia here: The article says the review was conducted by a toxicologist at the Pacific Northwest national Laboratory. BPA can mimic estrogen. The researcher, Justin Teeguarden, claimed BPA levels were too low to have an effect.
BPA is an ENDOCRINE DISRUPTOR. See here for definition
Endocrine disruptors are known to be capable of producing significant effects for developing beings, even at low levels, during critical developmental stages.
Let us look at some other studies that have show that fetal growth may be adversely linked to BPA and that BPA is linked to lower thyroid hormone levels in boys.
Fetal Growth and Prenatal Exposure to Bisphenol A: The Generation R Study Environmental Health Perspectives Claudia A. Snijder1,2, Dick Heederik3, Frank H. Pierik4, Albert Hofman1,5, Vincent W. Jaddoe1,5,6, Holger M. Koch7, Matthew P. Longnecker8, Alex Burdorf http://ehp.niehs.nih.gov/2013/01/1205296/
Background: Prenatal exposure to Bisphenol A (BPA) has been associated with adverse birth outcomes, but findings of previous studies have been inconsistent.
Objective: We investigate the relation of prenatal BPA exposure with intrauterine growth and evaluate the effect of the number of measurements per subject on observed associations.
Methods: This study was embedded in a Dutch population-based prospective cohort study, with urine samples collected during early, mid, and late pregnancy. The study comprised 219 women, of which 99 had one measurement, 40 had two measurements, and 80 had three measurements of urinary BPA. Fetal growth characteristics were repeatedly measured by ultrasound during pregnancy and combined with measurements at birth. Linear regression models for repeated measurements of both BPA and fetal growth were used to estimate associations between urinary concentrations of creatinine based BPA (BPACB) and intrauterine growth.
Results: The relationship between BPACB and fetal growth was sensitive to the number of BPA measurements per woman. Among 80 women with three BPA measurements, women with BPACB > 4.22 μg/g Crea had lower growth rates for fetal weight and head circumference than women with BPACB <1 -3.9="" -683="" .54="" and="" at="" attenuated="" available="" became="" birth="" cm="" crea="" differences="" estimated="" exposure-response="" fewer="" g="" grams="" in="" mean="" measurements="" nbsp="" non-significant.="" of="" per="" progressively="" relationship="" respectively.="" span="" statistically="" the="" values="" were="" when="" with="" woman="">1>
Conclusion: Our findings suggest that maternal urinary BPA may impair fetal growth. Since previous studies have shown contradictory findings, further evidence is needed to corroborate these findings in the general population.
Maternal Urinary Bisphenol A during Pregnancy and Maternal and Neonatal Thyroid Function in the CHAMACOS Study 1/2/2013 Jonathan Chevrier,1 Robert B. Gunier,1 Asa Bradman,1 Nina T. Holland,1 Antonia M. Calafat,2 Brenda Eskenazi,1 and Kim G. Harleyhttp://ehp.niehs.nih.gov/2013/01/1205092/
Abstract Background: Bisphenol A (BPA) is widely used in the manufacture of polycarbonate plastic bottles, food and beverage can linings, thermal receipts, and dental sealants. Animal and human studies suggest that BPA may disrupt thyroid function. Although thyroid hormones play a determinant role in human growth and brain development, no studies have investigated relations between BPA exposure and thyroid function in pregnant women or neonates.
Objective: Our goal was to evaluate whether exposure to BPA during pregnancy is related to thyroid hormone levels in pregnant women and neonates.
Methods: We measured BPA concentration in urine samples collected during the first and second half of pregnancy in 476 women participating in the CHAMACOS (Center for the Health Assessment of Mothers and Children of Salinas) study. We also measured free thyroxine (T4), total T4, and thyroid-stimulating hormone (TSH) in women during pregnancy, and TSH in neonates.
Results: Associations between the average of the two BPA measurements and maternal thyroid hormone levels were not statistically significant. Of the two BPA measurements, only the one taken closest in time to the TH measurement was significantly associated with a reduction in total T4 (β = –0.13 µg/dL per log2 unit; 95% CI: –0.25, 0.00). The average of the maternal BPA concentrations was associated with reduced TSH in boys (–9.9% per log2 unit; 95% CI: –15.9%, –3.5%) but not in girls. Among boys, the relation was stronger when BPA was measured in the third trimester of pregnancy and decreased with time between BPA and TH measurements.
Conclusion: Results suggest that exposure to BPA during pregnancy is related to reduced total T4 in pregnant women and decreased TSH in male neonates. Findings may have implications for fetal and neonatal development.
Majia here: It seems to me that the Wall Street Journal headline is another LIE aimed at protecting polluters.
The true extent of effects of BPA has yet to be mapped, but it is clear that BPA has been shown capable of disrupting endocrine functions in developing beings. It is therefore not true that there are "no ill effects."