(searched for: doi:10.1016/j.scitotenv.2017.09.276)
Ecotoxicology and Environmental Safety, Volume 249; https://doi.org/10.1016/j.ecoenv.2022.114355
Chemosphere, Volume 312; https://doi.org/10.1016/j.chemosphere.2022.137265
Environmental Pollution, Volume 313; https://doi.org/10.1016/j.envpol.2022.120173
Environmental Science and Pollution Research, Volume 30, pp 4582-4591; https://doi.org/10.1007/s11356-022-22327-y
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Reviews on Environmental Health; https://doi.org/10.1515/reveh-2022-0077
Phthalates are a kind of synthetic plasticizers, which extensively used as plastic productions to improve their plasticity and flexibility. However, exposure to phthalates has been proved an increased risk of respiratory disease, because by they affect the development and functions of the lung and immune system. Here, we attempt to review respiratory health of phthalate exposure. Firstly, we describe the relationship between phthalates and lung function and airway inflammation. Then, the role of phthalates in asthma, lung cancer, rhinitis, and respiratory tract infections and the possible mechanisms of action are discussed. Finally, possible effective measures to reduce exposure to phthalates are proposed, and health care workers are called upon to provide educational resources and advocate for informed public health policies. Overall, the evidence for association between phthalate exposure and respiratory disease is weak and inconsistent. Therefore, thorough implementation in large populations is needed to produce more consistent and robust results and to enhance the overall understanding of the potential respiratory health risks of phthalate in long-term exposure.
Neurotoxicity Research, Volume 39, pp 1430-1439; https://doi.org/10.1007/s12640-021-00386-2
Long-term exposure to different types of chemicals is hazardous to human health. Di(2-ethylhexyl) phthalate (DEHP) could exert pleiotropic deleterious effects on nervous systems. Mono(2-ethylhexyl) phthalate (MEHP), as one of the most toxic metabolites of DEHP, may have similar effects on nervous systems. However, no effects of MEHP on neural circuits have been reported. To uncover the regulation of MEHP on neural transmission, the functional changes of neural excitability and synaptic plasticity of projection neurons (PNs) have been assessed. In the current study, we recorded the action potentials (APs), stimulate action potentials (sti-APs), mini excitement postsynaptic current (mEPSC), calcium currents, and sodium currents from PNs of isolated whole brain of Drosophila model utilizing patch clamp recordings. We found that MEHP-300 (at the concentration of 300 μM), but not MHEP-100 (at the concentration of 100 μM), significantly decreased the frequency and amplitude of APs. Besides, the amplitude and anti-amplitude of sti-APs were reduced with the application of MEHP-300. Meanwhile, MEHP-300 reduced the frequency of mEPSC, but not the amplitude. Furthermore, MEHP-300 reduced the peak current densities of sodium and calcium channels. Therefore, our results indicated that MEHP could alter the neural excitability and synaptic plasticity of PNs by inhibiting the ion channels activities, revealing the potential modulation of MEHP on neural transmission of PNs.
Toxicology in Vitro, Volume 73; https://doi.org/10.1016/j.tiv.2021.105148
Phthalates are widely used in polymer science and have potential toxicity related to their chemical structures. However, lots of evidence indicate that phthalate derivatives are undoubtedly produced as secondary metabolites by organisms, including plants, animals, and microorganisms. In the present study, Bacillus velezensis strain RP137 was cultured under optimized conditions. Its biomass was extracted with ethyl acetate with one fraction showing cytotoxic properties. A pure compound was isolated from the active fraction using combined silica gel and LH20 size exclusion column chromatography. Structural evaluation including FT-IR, 1H NMR, 13C NMR, HR-MS and CHN analysis identified the purified compound as di(2-ethylhexyl)phthalate (DEHP) with the formula C24H38O4 and the molecular weight of 389.29 Da. The microorganism-derived (stereospecific) DEHP was strongly reduced the proliferation and induced cytotoxic effects on various eukaryotic cell lines in compare to the synthetic racemic mixture of the compound when assessed by MTT assay. Furthermore, crystal violet assay and morphological changes confirmed the cytotoxic effect of DEHP. Interestingly, non-malignant SV40-immortalized fibroblast cells were less affected by the purified DEHP. Further evaluation on the antibacterial activity of DEHP documented no effect toward Gram-positive (S. aureus) and Gram-negative (E. coli and P. aeruginosa) pathogens even at a high concentration of 100 μM. In conclusion, existence of DEHP as byproduct of microorganism's metabolism can seriously be considered as a warning to human health.
Environmental Science and Pollution Research, Volume 28, pp 27333-27344; https://doi.org/10.1007/s11356-020-12322-6
Phthalates can leach into indoor and outdoor airborne particulate matter and dust, which can then be ingested or absorbed and induce lung injury. Dermal phthalate levels can be used as a matrix for exposure direct absorption from air, particle deposition, and contact with contaminated products. However, the association between dermal phthalate levels in skin wipes and lung function tests remains unknown. A total of 397 participants were included. Spirometry measurements of forced expiratory volume in 1 s (FEV1, L) and forced vital capacity (FVC, L) were calculated. Dermal phthalate levels of diethyl phthalate (DMP), diethyl phthalate (DEP), di(n-butyl) phthalate (DnBP), butyl benzyl phthalate (BBzP), di(2-ethylhexyl) phthalate (DEHP), diisononyl phthalate (DiNP), and diisodecyl phthalate (DiDP) on forehead skin wipes were detected. The one-unit increases in logarithm (log) dermal DnBP (β = − 0.08; 95% CI − 0.16, − 0.003, p = 0.041), BBzP (β = − 0.09; 95% CI − 0.16, − 0.02, p = 0.009), DEHP (β = − 0.07; 95% CI − 0.14, − 0.003, p = 0.042), and DiNP (β = − 0.08; 95% CI − 0.15, − 0.02, p = 0.017) were significantly associated with decreases in FVC. For elderly participants, one-unit increases in log dermal DnBP (β = − 0.25; 95% CI − 0.46, − 0.04, p = 0.021), BBzP (β = − 0.17; 95% CI − 0.33, − 0.01, p = 0.042), and DiDP (β = − 0.19; 95% CI − 0.39, < 0.01, p = 0.052) were associated with decreases in FEV1. In conclusion, dermal phthalate levels were significantly associated with decreases in lung function tests.
Environmental Research, Volume 194; https://doi.org/10.1016/j.envres.2020.110613
Phthalate concentrations in indoor and outdoor dust are associated with respiratory disease. Both immunoglobulin E (IgE) and eosinophil count are associated with airway inflammation from exposure to environmental allergens. Dermal phthalate level can be used as a matrix for assessing personal exposure through direct absorption from the air, particle deposition, or contact with contaminated products. However, the association between dermal phthalate level and changes in lung function test values, as mediated by immunological response, remains unclear. In total, 237 adults in southern Taiwan were recruited. Spirometry measurements (in L) of forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) were taken on visits 1 (2016–2018) and 2 (2019). Dermal phthalate level, absolute eosinophil count, and IgE level were recorded on visit 1. Mean changes in FVC and FEV1 decrease pear year, as determined through pairwise comparisons, were significant (diffFVCper year: −0.46, 95% CI: −0.51, −0.41; p < 0.001; diffFEV1per year: −0.37, 95% confidence interval [CI]: −0.41, −0.34; p < 0.001). For FEV1 decrease, log-unit increases in dermal diethyl phthalate (DEP) were positively associated with diffFEV1per year (β = 0.096; 95% CI: 0.042, 0.150; p = 0.001) and negatively associated with absolute eosinophil count (β= −0.201; 95% CI: −0.380, −0.023; p= 0.027). Log-unit increases in absolute eosinophil count were negatively associated with diffFEV1per year (β= −0.109; 95% CI: −0.150, −0.068; p < 0.001). Absolute eosinophil count mediated 19.70% of the association between dermal DEP level and diffFEV1per year. For FVC decrease, log-unit increases in dermal DEP were positively associated with diffFVCper year (β = 0.095; 95% CI: 0.035, 0.155; p = 0.002) and negatively associated with absolute eosinophil count (β = −0.243; 95% CI: −0.427, −0.060; p = 0.010). Log-unit increases in absolute eosinophil count were negatively associated with diffFVCper year (β= −0.122; 95% CI: −0.168, −0.076; p < 0.001). Absolute eosinophil count mediated 29.98% of the association between dermal DEP level and diffFVCper year. The results suggest that dermal DEP level is positively associated with changes in lung function test values and is mediated by absolute eosinophil count.
Journal of Hazardous Materials, Volume 406; https://doi.org/10.1016/j.jhazmat.2020.124316
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Environment International, Volume 143; https://doi.org/10.1016/j.envint.2020.105970
Environmental Pollution, Volume 267; https://doi.org/10.1016/j.envpol.2020.115564
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Environment International, Volume 139; https://doi.org/10.1016/j.envint.2020.105706
Phthalates are among the most ubiquitous environmental contaminants and endocrine-disrupting chemicals. Exposure to phthalates and related health effects have been extensively studied over the past four decades. An association between phthalate exposure and allergic diseases has been suggested, although the literature is far from conclusive. This article reviews and evaluates epidemiological (n = 43), animal (n = 49), and cell culture studies (n = 42), published until the end of 2019, on phthalates and allergic diseases, such as asthma, rhinoconjunctivitis, and eczema. In contrast to earlier reviews, emphasis is placed on experimental studies that use concentrations with relevance for human exposure. Epidemiological studies provide support for associations between phthalate exposures and airway, nasal, ocular, and dermal allergic disease outcomes, although the reported significant associations tend to be weak and demonstrate inconsistencies for any given phthalate. Rodent studies support that phthalates may act as adjuvants at levels likely to be relevant for environmental exposures, inducing respiratory and inflammatory effects in the presence of an allergen. Cell culture studies demonstrate that phthalates may alter the functionality of innate and adaptive immune cells. However, due to limitations of the applied exposure methods and models in experimental studies, including the diversity of phthalates, exposure routes, and allergic diseases considered, the support provided to the epidemiological findings is fragmented. Nevertheless, the current evidence points in the direction of concern. Further research is warranted to identify the most critical windows of exposure, the importance of exposure pathways, interactions with social factors, and the effects of co-exposure to phthalates and other environmental contaminants.
Toxicology Mechanisms and Methods, Volume 30, pp 427-437; https://doi.org/10.1080/15376516.2020.1758980
Di-(2-ethylhexyl) phthalate (DEHP) and its main metabolite, monoethylhexyl phthalic acid (MEHP), are a serious threat to human and animals’ health in the current century. However, their exact mechanism to induce nephrotoxicity is not clear. In the current study, we addressed toxic effects of MEHP and DEHP on embryonic human kidney cells (HEK-293 cell line) and kidney tissue of rats, respectively. In the HEK-293, MTT assay and oxidative stress parameters were measured after treatment with different concentrations of MEHP. For in vivo study, rats were treated with different doses of DEHP (50, 100, 200, 400 mg/kg) via gavage administration for 45 days. The renal function biomarkers (BUN and creatinine) were determined in serum of rats. Mitochondrial toxic parameters including MTT, mitochondrial membrane potential (MMP), mitochondrial swelling, and also oxidative stress parameters were measured in isolated kidney mitochondria. Histopathological effects of DEHP were also evaluated in rats’ kidneys. We demonstrated that MEHP induced oxidative stress and cytotoxicity in HEK-293 cells in a concentration dependent manner. The administration of DEHP led to histopathological changes in kidney tissue, which concurred with BUN and creatinine alternations in serum of rats. The results of present study showed a significant mitochondrial dysfunction and oxidative stress confirmed by enhancement of mitochondrial swelling, mitochondrial reactive oxygen species (ROS) and malondialdehyde (MDA), and reduction of MMP and mitochondrial glutathione (GSH). Taken together, this study showed that DEHP/MEHP resulted in mitochondrial dysfunction and oxidative damage, which suggest a vital role of mitochondria in DEHP/MEHP-induced nephrotoxicity.
Epigenetics Insights, Volume 13; https://doi.org/10.1177/2516865720939971
Phthalate plasticizers are ubiquitous chemicals linked to several cardiovascular diseases in animal models and humans. Despite this, the mechanisms by which phthalate exposures cause adverse cardiac health outcomes are unclear. In particular, whether phthalate exposures during pregnancy interfere with normal developmental programming of the cardiovascular system, and the resulting implications this may have for long-term disease risk, are unknown. Recent studies suggest that the effects of phthalates on metabolic and neurobehavioral outcomes are sex-specific. However, the influence of sex on cardiac susceptibility to phthalate exposures has not been investigated. One mechanism by which developmental exposures may influence long-term health is through altered programming of DNA methylation. In this work, we utilized an established mouse model of human-relevant perinatal exposure and enhanced reduced representation bisulfite sequencing to investigate the long-term effects of diethylhexyl phthalate (DEHP) exposure on DNA methylation in the hearts of adult male and female offspring at 5 months of age (n = 5-7 mice per sex and exposure). Perinatal DEHP exposure led to hundreds of sex-specific, differentially methylated cytosines (DMCs) and differentially methylated regions (DMRs) in the heart. Pathway analysis of DMCs revealed enrichment for several pathways in females, including insulin signaling, regulation of histone methylation, and tyrosine phosphatase activity. In males, DMCs were enriched for glucose transport, energy generation, and developmental programs. Notably, many sex-specific genes differentially methylated with DEHP exposure in our mouse model were also differentially methylated in published data of heart tissues collected from human heart failure patients. Together, these data highlight the potential role for DNA methylation in DEHP-induced cardiac effects and emphasize the importance of sex as a biological variable in environmental health studies.
Efsa Journal, Volume 17; https://doi.org/10.2903/j.efsa.2019.5838
The EFSA Panel on Food Contact Materials, Enzymes and Processing Aids (CEP Panel) was asked by the European Commission to update its 2005 risk assessments of di‐butylphthalate (DBP), butyl‐benzyl‐phthalate (BBP), bis(2‐ethylhexyl)phthalate (DEHP), di‐isononylphthalate (DINP) and di‐isodecylphthalate (DIDP), which are authorised for use in plastic food contact material (FCM). Dietary exposure estimates (mean and high (P95)) were obtained by combining literature occurrence data with consumption data from the EFSA Comprehensive Database. The highest exposure was found for DINP, ranging from 0.2 to 4.3 and from 0.4 to 7.0 μg/kg body weight (bw) per day for mean and high consumers, respectively. There was not enough information to draw conclusions on how much migration from plastic FCM contributes to dietary exposure to phthalates. The review of the toxicological data focused mainly on reproductive effects. The CEP Panel derived the same critical effects and individual tolerable daily intakes (TDIs) (mg/kg bw per day) as in 2005 for all the phthalates, i.e. reproductive effects for DBP (0.01), BBP (0.5), DEHP (0.05), and liver effects for DINP and DIDP (0.15 each). Based on a plausible common mechanism (i.e. reduction in fetal testosterone) underlying the reproductive effects of DEHP, DBP and BBP, the Panel considered it appropriate to establish a group‐TDI for these phthalates, taking DEHP as index compound as a basis for introducing relative potency factors. The Panel noted that DINP also affected fetal testosterone levels at doses around threefold higher than liver effects and therefore considered it conservative to include it within the group‐TDI which was established to be 50 μg/kg bw per day, expressed as DEHP equivalents. The aggregated dietary exposure for DBP, BBP, DEHP and DINP was estimated to be 0.9–7.2 and 1.6–11.7 μg/kg bw per day for mean and high consumers, respectively, thus contributing up to 23% of the group‐TDI in the worst‐case scenario. For DIDP, not included in the group‐TDI, dietary exposure was estimated to be always below 0.1 μg/kg bw per day and therefore far below the TDI of 150 μg/kg bw per day. This assessment covers European consumers of any age, including the most sensitive groups. Based on the limited scope of the mandate and the uncertainties identified, the Panel considered that the current assessment of the five phthalates, individually and collectively, should be on a temporary basis.
Environmental Pollution, Volume 257; https://doi.org/10.1016/j.envpol.2019.113593
Di (2-ethyl-hexyl)phthalate (DEHP) is an environmental endocrine disruptor and commonly used as plasticizer. Maternal DEHP exposure during pregnancy reduces placental size and destroys placental structure. However, the underlying mechanisms were unclear. In this study, we supposed that DEHP disturbs endocrine function of placenta to inhibit the proliferation of placental cell. Using radioimmunoassay and ELISA, we found that DEHP and its active metabolite mono (2-ethyl-hexyl) phthalate (MEHP) promoted progesterone secretion in pregnant mouse and in JEG-3 cells, respectively. Therefore, placental endocrine function was altered by DEHP. The mRNA and protein level of progesterone synthetase 3β-HSD1 was elevated by DEHP, which is conducive to the synthesis of progesterone. The level of progesterone receptor was down-regulated by DEHP and MEHP in mouse placenta and in JEG-3 cells, respectively. PR deficiency further promoted the level of 3β-HSD1, which leads to a higher progesterone level. In turn, higher concentration of progesterone further inhibited the expression of PGR (PR gene). Therefore, higher progesterone down-regulated the level of its receptor PR. Meanwhile, decreased PR induced more progesterone secretion. There is a feedback loop between progesterone and PR. PR deficiency down-regulated the protein level of Cyclin D1 which plays an important role in cell proliferation. Accordingly, DEHP and its active metabolite MEHP can restrain proliferation of placental cell and disturb the progesterone secretion via decreasing the level of PR.
Environmental Science and Pollution Research, Volume 26, pp 28256-28269; https://doi.org/10.1007/s11356-019-06003-2
Environmental exposure to phthalates may contribute to an increased risk of asthma in children and adults. We aimed to assess the direction and strength of the association between urinary phthalates metabolites and current asthma in children and adults that participated in the National Health and Nutrition Examination Survey (NHANES) 2007–2012. Data on ten urinary phthalate metabolites, self-reported questionnaires, spirometry measures, and covariates were obtained from 7765 participants (28.1% were children aged 6–17 years) taking part in the NHANES 2007–2012. Asthma was assessed using self-reported questionnaires for children and adults, and via spirometry measures for adults alone. We used crude and adjusted logistic regression models to estimate the odds ratios (ORs) and 95% confidence interval (CI) per one log10 unit change in the concentration of phthalate metabolites. We further modeled the effect modification by sex. Out of 10 metabolites, only mono-benzyl phthalate (MBzP) was positively associated with the prevalence of self-reported asthma in children, after adjusting for a range of potential confounders (odds ratio 1.54; 95% confidence interval 1.05–2.27). No significant relationship was observed for adults. The association of mono-ethyl phthalate (MEP) was modified by sex, with significantly increased odds of asthma among males [boys (2.00; 1.14–3.51); adult males (1.32; 1.04–1.69)]. While no other phthalates showed a positive relationship with current asthma in males, mono-(carboxynonyl) phthalate (MCNP) and mono-(3-carboxylpropyl) phthalate (MCPP) were inversely associated with spirometrically defined asthma in adult females. A sex-specific relationship in adults was evident when spirometry, but not self-reported measures were used to define asthma. We found no clear association between exposure to phthalates and current asthma, except for a significant relationship between MBzP metabolites and self-reported asthma in children. As a result, exposure to phthalates and asthma development and/or exacerbations remains controversial, suggesting a need for a well-designed longitudinal study.
Published: 26 June 2019
Frontiers in Cellular and Infection Microbiology, Volume 9; https://doi.org/10.3389/fcimb.2019.00221
Diethylhexylphthalate (DEHP), acting as an endocrine disruptor, disturbed reproductive health. Here, we evaluated the effects of Lactobacillus plantarum TW1-1 (L. plantarum TW1-1) on DEHP-induced testicular damage in adult male mice. Results showed that oral supplementation of L. plantarum TW1-1 significantly increased the serum testosterone concentration, enhanced the semen quality, and attenuated gonad development defects in DEHP-exposed mice. L. plantarum TW1-1 also alleviated DEHP-induced oxidative stress and inflammatory responses by decreasing the mRNA expression and serum protein concentration of different inflammatory factors [tumor necrosis factor-α, interleukin (IL)-1β and IL-6]. Furthermore, L. plantarum TW1-1 significantly reduced DEHP-induced intestinal hyper-permeability and the increase in the serum lipopolysaccharide level. Gut microbiota diversity analysis revealed that L. plantarum TW1-1 shifted the DEHP-disrupted gut microbiota to that of the control mice. At phylum level, L. plantarum TW1-1 reversed DEHP-induced Bacteroidetes increase and Firmicutes decrease, and restored Deferribacteres in DEHP-exposed mice. Spearman's correlation analysis showed that Bacteroidetes, Deferribacteres, and Firmicutes were associated with DEHP-induced testicular damage. In addition, the ratio of Firmicutes to Bacteroidetes (Firm/Bac ratio) significantly decreased from 0.28 (control group) to 0.13 (DEHP-exposed group), which was restored by L. plantarum TW1-1 treatment. Correlation analysis showed that the Firm/Bac ratio was negatively correlated with testicular damage and inflammation. These findings suggest that L. plantarum TW1-1 prevents DEHP-induced testicular damage via modulating gut microbiota and decreasing inflammation.
Environmental Toxicology and Pharmacology, Volume 67, pp 53-60; https://doi.org/10.1016/j.etap.2019.01.012
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Chemosphere, Volume 215, pp 313-322; https://doi.org/10.1016/j.chemosphere.2018.10.040
Di-(2-ethylhexyl) phthalate (DEHP) is an endocrine disrupting chemical (EDC) widely used as a plasticizer in many materials. Epidemiological investigations have shown that DEHP exposure during early development is related to cerebellar-related adverse neurodevelopmental outcomes. However, animal studies involving the effect of DEHP exposure on cerebellar development have rarely been reported and the potential mechanisms are unclear. The aim of this study was to investigate the effect of maternal DEHP exposure on the proliferation of cerebellar granule cell precursor cells (GCPs) and the mechanisms involved. Wistar rats were randomly assigned to four exposure groups and given 0, 30, 300, or 750 mg/kg/d DEHP by intragastric administration from gestational day (GD) 0 to postnatal day (PN) 21. Exposure to 300 and 750 mg/kg/d DEHP restrained GCPs proliferation and impaired neurodevelopment for males. Furthermore, exposure to 300 and 750 mg/kg/d DEHP decreased male pups protein expressions and mRNA levels of molecules related to proliferation, including Shh, Gli1, N-Myc, CyclinD1. In addition, the estrogen level and aromatase expression also reduced in male pups after maternal exposure to DEHP. However, effects on females were not obvious. These results suggested that 300 and 750 mg/kg/d DEHP exposure inhibit the proliferation of GCPs in male offspring and ultimately contribute to the impairment of neuromotor development. This, may be caused by the down-regulation of Shh signaling. And the susceptibility of male offspring to DEHP exposure may be attributed to the decreased estrogen level and aromatase expression in male pup's cerebellum.
Published: 31 December 2018
Journal: Experimental Neurobiology
Experimental Neurobiology, Volume 27, pp 472-488; https://doi.org/10.5607/en.2018.27.6.472
Di-(2-ethylhexyl) phthalate (DEHP) is an ubiquitous environmental contaminant because of its extensive use in plastics and its persistence. As an environmental endocrine disruptor, it is suspected to interfere with neurodevelopment in people. However, evidence of the effects of maternal DEHP exposure on cerebellar development in offspring is scarce. The objective of this study was to investigate maternal exposure to DEHP and its effect on apoptosis of cerebellar granule cells (CGCs) and related mechanisms. Pregnant Wistar rats were administrated DEHP (0, 30, 300 and 750 mg/kg/d) by gavage from gestational day (GD) 0 to postnatal day (PN) 21. Primary CGCs were also exposed to mono-(2-ethylhexyl) phthalate (MEHP), the main metabolite of DEHP, for 24 h with concentrations of 0, 25, 100 and 250 µM. The CGCs of male offspring from 300 and 750 mg/kg/d DEHP exposure groups showed significantly increased apoptosis. In addition, the PI3K/AKT signaling pathway was inhibited in the male offspring of the 300 and 750 mg/kg/d DEHP exposure groups. However, effects on female pups were not obvious. Apoptosis was also elevated and the PI3K/AKT signaling pathway was inhibited after primary CGCs were exposed to MEHP. Furthermore, apoptosis was reduced after treatment with the PI3K/AKT signaling pathway activator, insulin-like growth factor (IGF) 1, and increased after treatment with LY294002, an inhibitor of the PI3K/AKT signaling pathway. These results suggested that maternal DEHP exposure induced apoptosis in the CGCs of male pups via the PI3K/AKT signaling pathway, and the apoptosis could be rescued by IGF1 and aggravated by LY294002.
Science of the Total Environment, Volume 656, pp 862-869; https://doi.org/10.1016/j.scitotenv.2018.11.458
The occurrence and fate of nine phthalate esters (PAEs), including dimethyl phthalate (DMP), diethyl phthalate (DEP), di‑n‑butyl phthalate (DBP), di-isobutyl phthalate (DIBP), benzyl butyl phthalate (BzBP), di (2‑ethylhexyl) phthalate (DEHP), di‑n‑hexyl phthalate (DNHP), dicyclohexyl phthalate (DCHP), and di‑n‑octyl phthalate (DNOP), in sludges collected from 46 wastewater treatment plants (WWTPs) from 22 Chinese provinces were investigated. The nine PAEs were detected in almost all the sludge samples. DEHP was the most abundant congener in all sludge samples, followed by DBP and DIBP. The DEHP concentrations in sludge were in the range of 0.326–67.8 (mean: 14.7) μg/g dry weight (dw), which were at the lower bound or middle of the concentration range of DEHP in sludge globally (0.0200–3514 μg/g dw). Spatial distribution and mass loading of PAEs in WWTPs were investigated. The concentrations of Σ9PAEs in sludges from different provinces were in the order as follows: Jilin (40.2 μg/g dw) > Liaoning (38.9 μg/g dw) > Beijing (30.7 μg/g dw), while the mass loading of ∑9PAEs in sludges were Guangdong (10.1 tons/yr) > Liaoning (9.97 tons/yr) > Shandong (5.59 tons/yr). Our study showed that the geographical distribution of PAEs in sludges was similar to that in indoor dusts found in earlier study, suggesting the existence of a common source for these chemicals in both matrices. Based on the concentrations measured, human exposure to PAEs through sludge application in soil was evaluated and the exposure dose is minor.
Frontiers in Neuroscience, Volume 12; https://doi.org/10.3389/fnins.2018.00444
Di-(2-ethylhexyl) phthalate (DEHP), as a prevalent xenoestrogen endocrine disrupter, is omnipresent in the environment and commonly used in polyethylene plastic products. Although DEHP has potential adverse effects on multisystem organs, damage to the central nervous system is more significant. However, the consequences and mechanisms of DEHP exposure remain to be explored. The aim of this study was to investigate the effects and related mechanisms of maternal DEHP exposure on dendritic development of hippocampal pyramidal neurons in a rat model. Pregnant Wistar rats were intragastrically administrated either vehicle or DEHP (30, 300, and 750 mg/kg/d) from gestation day 0 to postnatal day (PN) 21. The dendritic length and complexity of dendritic arbors’ pattern in pyramidal neurons of the hippocampus were measured using Golgi–Cox staining and Sholl analysis. The expression of dendritic development-related proteins was detected using western blot and immunofluorescence staining. DEHP-treated male but not female pups showed an obvious decrease in the total length and branching numbers of basal dendrites on PN7, PN14, and PN21. The phosphorylation of MAP2c, stathmin, and JNK1 in the male pup hippocampus was significantly decreased in DEHP treatment groups compared to controls. However, protein expression alteration in the hippocampus of female offspring was not observed. In summary, our study indicated that DEHP has a gender-specific negative impact on the dendritic growth of CA1 pyramidal neurons in male offspring of a rat model of DEHP exposure. The adverse impact may be related to the dysregulation of phosphorylated and total MAP2c and stathmin mediated by JNK1.
Environment International, Volume 115, pp 79-88; https://doi.org/10.1016/j.envint.2018.03.016
Prenatal bisphenol A and paradichlorobenzene exposures were associated with pediatric respiratory outcomes among boys. Future studies may shed light on biological mechanisms and potential sexually-dimorphic effects of select phenols and phthalates on respiratory disease development.
Published: 24 May 2018
Archives of Environmental Contamination and Toxicology, Volume 75, pp 145-156; https://doi.org/10.1007/s00244-018-0535-9
Di-(2-ethylhexyl) phthalate (DEHP) is a plasticizer used in the polyvinyl chloride industry worldwide. DEHP exists in the aquatic environments for decades. However, the toxicological effects of DEHP to aquatic organisms have not been adequately researched. We investigated acute toxicity, oxidative damage, antioxidant enzyme activities, and gene expression patterns of antioxidant enzymes in juvenile and adult Daphnia magna exposed to DEHP. We found that the median lethal concentrations (LC50) of DEHP for juveniles exposed for 24 and 48 h were 0.83 and 0.56 mg L−1, respectively. The LC50 of DEHP in adults exposed for 24 and 48 h were 0.48 and 0.35 mg L−1. Daphnia magna that was exposed to DEHP had increased malondialdehyde levels for 24 h and lower total antioxidant capacity compared with the control. Activity levels of antioxidant enzymes superoxide dismutase and phase II detoxifying enzyme glutathione S-transferases were significantly higher upon initial exposure for 24 h, and enzyme activity was then diminished at high concentrations and prolonged exposure for 48 h. Gene expression levels of cat and gst were notably reduced or increased upon DEHP exposure. These findings suggest that DEHP can cause biochemical and physiological effects in juvenile and adult D. magna by inhibiting enzymes, an increase in lipid peroxidation levels and changes both transcription levels of enzymes (cat, gst). On the whole, juveniles and adults both responded similarly to DEHP. Our findings will contribute to the understanding of toxic mechanisms in phthalate esters and the evaluation of environmental risks in aquatic ecosystems.