The plasticizer market: an assessment of traditional plasticizers and research trends to meet new challenges

Molecular, clinical, and environmental toxicolog , Molecular, clinical, and environmental toxicolog , کتابخانه دیجیتال جندی شاپور اهواز

Molecular, Clinical and Environmental Toxicology

The purposes of this review are to (1) evaluate human and experimental evidence for adverse effects on reproduction and development in humans, produced by exposure to phthalates, and (2) identify knowledge gaps as for future studies. The widespread use of phthalates in consumer products leads to ubiquitous and constant exposure of humans to these chemicals. Phthalates were postulated to produce endocrine-disrupting effects in rodents, where fetal exposure to these compounds was found to induce developmental and reproductive toxicity. The adverse effects observed in rodent models raised concerns as to whether exposure to phthalates represents a potential health risk to humans. At present, di(2-ethylhexyl) phthalate (DEHP), di-n-butyl phthalate (DBP), and butyl benzyl phthalate (BBP) have been demonstrated to produce reproductive and developmental toxicity; thus, this review focuses on these chemicals. For the general population, DEHP exposure is predominantly via food. The average concentrations of phthalates are highest in children and decrease with age. At present, DEHP exposures in the general population appear to be close to the tolerable daily intake (TDI), suggesting that at least some individuals exceed the TDI. In addition, specific high-risk groups exist with internal levels that are several orders of magnitude above average. Urinary metabolites used as biomarkers for the internal levels provide additional means to determine more specifically phthalate exposure levels in both general and high-risk populations. However, exposure data are not consistent and there are indications that secondary metabolites may be more accurate indicators of the internal exposure compared to primary metabolites. The present human toxicity data are not sufficient for evaluating the occurrence of reproductive effects following phthalate exposure in humans, based on existing relevant animal data. This is especially the case for data on female reproductive toxicity, which are scarce. Therefore, future research needs to focus on developmental and reproductive endpoints in humans. It should be noted that phthalates occur in mixtures but most toxicological information is based on single compounds. Thus, it is concluded that it is important to improve the knowledge of toxic interactions among the different chemicals and to develop measures for combined exposure to various groups of phthalates.

Reproductive and Developmental Toxicity of Phthalates

Di-(2-ethylhexyl)phthalate (DEHP), the most commonly used plasticizer in flexible polyvinylchloride formulations, is a ubiquitous environmental contaminant. To date, no information exists on the potential health hazards from exposure to DEHP and/or its main metabolite, mono-(2-ethylhexyl)phthalate (MEHP), in high-risk conditions, such as pregnancy and during the neonatal period. The aim of this study was to evaluate prenatal exposure to DEHP and/or MEHP and its possible biologic effects. We measured serum DEHP and MEHP concentrations in the cord blood of 84 consecutive newborns by high-performance liquid chromatography. Relationships between DEHP/MEHP and infant characteristics were tested using Fisher's exact test, unpaired t-tests, and univariate linear regression analyses, and significant differences on univariate analysis were evaluated using multiple logistic regression analysis. We found detectable cord blood DEHP and/or MEHP concentrations in 88.1% of the samples. Either DEHP or MEHP was present in 65 of 84 (77.4%) of the examined samples. Mean concentrations of DEHP and MEHP were 1.19 +/- 1.15 microg/mL [95% confidence interval (CI), 0.93-1.44, range = 0-4.71] and 0.52 +/- 0.61 microg/mL (95% CI, 0.39-0.66, range = 0-2.94), respectively. MEHP-positive newborns showed a significantly lower gestational age compared with MEHP-negative infants (p = 0.033). Logistic regression analysis results indicated a positive correlation between absence of MEHP in cord blood and gestational age at delivery (odds ratio = 1.50, 95% CI, 1.013-2.21; p = 0.043). These findings confirm that human exposure to DEHP can begin in utero and suggest that phthalate exposure is significantly associated with a shorter pregnancy duration.

In utero exposure to di-(2-ethylhexyl)phthalate and duration of human pregnancy.

Case reports and review of the literature

Introduction: Our team investigated the etiology of total parenteral nutrition (TPN)-induced cholestasis, particularly concerning premature infants. The reason for TPN-induced cholestasis is still unknown. A multifactorial etiology is assumed. During our research we focussed on plasticizers, especially diethylhexylphthalate (DEHP), existing in PVC infusion lines, commonly used since the introduction of TPN. We discovered that the cholestasis parameter improved after breaking off lipid infusions. The aim of this study was to find a correlation between lipids and PVC infusion lines in TPN-induced cholestasis. Material and Methods: Infusion systems used for newborns on the ICU were perfused with TPN infusions (lipids, glucose, amino acids, packet red cells). The perfused solutions were collected and the DEHP concentrations were measured by gas chromatographic methods. The room temperatures were modified because of the higher temperature on the newborn ICU. Results: We found that the amount of extracted plasticizer from PVC lines increased with the lipophilia of the perfused solution. Glucose and amino acid solutions extracted low amounts of DEHP, but lipid solutions extracted high amounts of plasticizer, so that the total load of a newborn with DEHP reaches up to 10 mg a day (Table 1 ). The amount of extraction increases with the room temperature. Discussion: An extraction of DEHP from food packaging [1], blood product bags [2] and dialysis lines [3], consisting of PVC, is already known and leads to a loading of the human organism with DEHP. This study showed a comparable extraction of DEHP from commonly used PVC infusion lines. The toxicity of DEHP in humans is less known. Studies with rodents show a cancerogenity and genotoxicity, but this toxicity is probably not transferable to humans. It is known from cell studies that DEHP modulates enzyme systems [4], and the histological examination of liver cells from newborns suffering from TPN-induced cholestasis showed that the etiology of this damage is of a toxic nature. Relevant amounts of DEHP for immature and less developed infants with decreased enzyme functions may toxify drugs by enzyme modulation and may lead to the well-known liver damage. Further studies are necessary to confirm this hypothesis.

Besteht ein Zusammenhang zwischen der TPN-induzierten Cholestase bei Neugeborenen und der Herauslösung von Weichmachern aus Infusionslösungen?

Polyvinylchloride infusion lines expose infants to large amounts of toxic plasticizers

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Besteht ein Zusammenhang zwischen der TPN-induzierten Cholestase bei Neugeborenen und der Herauslösung von Weichmachern aus Infusionslösungen?

Polyvinylchloride infusion lines expose infants to large amounts of toxic plasticizers