Phthalate exposure among pregnant women in Jerusalem, Israel: results of a pilot study.
ABSTRACT Phthalates can disrupt endocrine function and induce reproductive and developmental toxicity in laboratory animals. Few studies have evaluated exposure to phthalates in pregnant women, despite the potential sensitivity of the developing fetus to adverse effects of phthalates.
We measured urinary concentrations of 11 phthalate metabolites in 19 pregnant women, recruited in Jerusalem, Israel in 2006, and collected questionnaire data on demographic factors and consumer habits from these women. We compared geometric mean concentrations in subgroups and used the Mann-Whitney U-test for independent samples to determine significant differences between groups.
Nine metabolites were detected in at least 95% of the samples: mono(2-ethyl-5-carboxypentyl) phthalate, mono(2-ethyl-5-hydroxyhexyl) phthalate, mono(2-ethyl-5-oxohexyl) phthalate, mono(3-carboxypropyl) phthalate, mono(n-butyl) phthalate, monobenzyl phthalate (MBzP), monoethyl phthalate (MEP), mono(2-ethylhexyl) phthalate and monoisobutyl phthalate. Phthalate metabolite concentrations in these pregnant women were remarkably similar to those in the general United States female population. MBzP geometric mean concentrations were higher in women living in buildings existing 40 years or more (P=0.04). In women who used four or more personal care products (perfume, deodorant, lipstick, nail polish, or hand/face cream) in the 48 h prior to providing the urine sample, geometric mean MEP concentrations were more than 4 times higher than concentrations in women using only two or three of the aforementioned products (P=0.07).
Pregnant women in Jerusalem are exposed to a wide range of phthalates. Building materials used in old constructions may be a source of exposure to benzylbutyl phthalate, the parent compound of MBzP. Personal care products may be sources of exposure to diethyl phthalate, the parent compound of MEP.
- SourceAvailable from: Zvi RothSociety for reproduction and fertility SRF; 07/2013
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ABSTRACT: In the last decade, potential exposure of humans and animals to industrial chemicals and pesticides has been a growing concern. In the present study, di-(2-ethylhexyl) phthalate (DEHP) and mono-(2-ethylhexyl) phthalate (MEHP) were used to model the effects of endocrine-disrupting compounds and their risk in relation to early embryonic losses. Exposure of cumulus oocyte complexes during maturation to 50 μM MEHP reduced the proportion of oocytes that underwent nuclear maturation (p < 0.05) and increased the proportion of apoptotic oocytes (p < 0.05). Furthermore, phthalates reduced cleavage rate in the MEHP-treated group (p < 0.05) and the proportion of embryos developing to the blastocyst stage in both DEHP- and MEHP-treated groups (p < 0.05). The total cell count for blastocysts developing from MEHP-treated oocytes was lower than in controls (p < 0.05). Exposure of oocytes to MEHP during maturation reduced (p < 0.05) the expression of ASAH1 (an anti-apoptotic factor), CCNA2 (involved in cell cycle control), and POU5F1 (responsible for pluripotency) in matured oocytes. Furthermore, the reduced mRNA expression of POU5F1 and ASAH1 lasted into two-cell stage embryos (p < 0.05). Phthalate-induced alterations in POU5F1, ASAH1, and CCNA2 expression might explain in part the reduced developmental competence of MEHP-treated oocytes.Cell Biology and Toxicology 09/2012; 28(6). DOI:10.1007/s10565-012-9230-1 · 1.97 Impact Factor
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ABSTRACT: Phthalates are industrial chemicals widely used in consumer products, plastics and children toys, and the risk of exposure to phthalates, especially prenatal exposure, is a growing concern justifying the development of an animal model to better understand their effect. The present study was designed to evaluate the suitability of a chick model for phthalate DEHP teratogenicity and neurobehavioral teratogenicity, a model which is simple and devoid of potential confounding factors such as maternal toxicity, maternal-fetal unit and maternal-neonatal interactions; major findings were confirmed in the DBP study. Prehatch exposure to DEHP in doses ranging from 20 to 100 mg/kg, reduced the percent hatching from 80% in control eggs to 65%, and increased late hatchings from 12.5% in control eggs to 29.4%. In addition it induced developmental defects characterized by an opening or weakening of abdominal muscles allowing internal organs to protrude externally with or without a sac, omphalocele or gastroschisis, respectively. The effect was dose dependent ranging from 8% with DEHP (20 mg/kg) to 22% (100 mg/kg). Similar treatment with DBP 100mg/kg has reduced percentage hatching to 57% and increased late hatching to 37.5%, with a 14% increase in gastroschisis. Biochemical evaluation revealed elevated levels of alkaline phosphatase, which reflects non-specific toxicity of DEHP at such a high dose. Behavioral evaluation using an imprinting test and locomotor activity on chicks pretreated with DEHP (100 mg/kg) has shown an abolishment of imprinting performance from the control (0.65) preference ratio. DNA damage measurements of the metabolite 8-hydroxydeoxyguanosine (8-OH-dG) in blood samples showed an increase of 39.7% after prehatch exposure to phthalates. This was statistically significant for DEHP and indicates genetic toxicity, since part of the teratogenic activity is associated with oxidative stress and DNA damage.Neurotoxicology and Teratology 02/2012; 34(1):56-62. DOI:10.1016/j.ntt.2011.10.001 · 3.22 Impact Factor