聚氯乙烯食品保鲜膜中己二酸二(2-乙基)己酯(DEHA)迁移量的测定

目的：选取去离子水、3％乙酸（w／v）水溶液、15％乙醇（v／v）水溶液和异辛烷作为食品模拟物进行迁移测试，采用气相色谱法测定聚氯乙烯膜中己二酸二（2-乙基）己酯（DEHA）向食品模拟物的迁移量。方法：异辛烷可以直接进样分析；其他水性食品模拟物经乙酸乙酯液液萃取后进样。采用非极性DB-1Ms毛细管气相色谱柱分离，氢火焰离子化检测器检测，以气相色谱质谱进行确证。结果：DEHA在1．0～100．0mg／L范围内线性相关系数为0．999，方法回收率在96．0％～106．4％之间，相对标准偏差小于5％，方法检测限为0．008mg／dm^2（水性食品模拟物）和0．005mg/dm^2（脂肪食品模拟物）。结论：检测结果表明，当PVC保鲜膜接触水性食品模拟物时，DEHA的迁移量小于0．8mg/dm^2；当接触脂肪食品模拟物时，DEHA的迁移量在1．46～4．23mg／dm^2之间。     

气相色谱-质谱法测定PVC食品保鲜膜中DEHA等己二酸酯类增塑剂

目的：介绍检验PVC食品保鲜膜中DEHA等己二酸酯类增塑剂的方法。方法：用异丙醇为提取溶剂，超声提取PVC食品保鲜膜中DEHA等己二酸酯类增塑剂，以己二酸二（1-丁基戊基）酯为内标采用GC-MS检测。结论：方法简便，重现性好，灵敏度高，定性、定量准确可靠。     

Induction of rat hepatic long-chain acyl-CoA hydrolases by various peroxisome proliferators

Induction of cytosolic long-chain acyl-CoA hydrolases was investigated in rat liver after administration of various peroxisome proliferators and related compounds. Treatment of rats with di-(2-ethylhexyl)-phthalate, di-(2-ethylhexyl)-adipate or tiadenol induced hydrolases I and II, while acetylsalicylic acid induced only hydrolase II. Among the various phenoxyacetic acid derivatives and related compounds, 2,4,5-trichlorophenoxyacetic acid, 2-(4-chlorophenoxy)-2-methylacetic acid, 2-(2-chlorophenoxy)-2-methylpropionic acid and clofibric acid induced both hydrolases I and II, whereas 2, 4-dichlorophenoxyacetic acid induced only hydrolase II. All nine of the above-mentioned inducers also markedly increased the activity of peroxisomal beta-oxidation. Other compounds tested (2-chlorophenoxyacetic acid, 4-chlorophenoxyacetic acid, 4-chlorophenol, phenoxyacetic acid and phenoxy-2-methylacetic acid) were ineffective as inducers. These results suggest that inducers of acyl-CoA hydrolase II also enhance peroxisomal beta-oxidation activity, but do not necessarily induce acyl-CoA hydrolase I. The structure-inducing activity relationships of these compounds are discussed.     

Elimination,distribution and metabolism of di-(2-ethylhexyl)adipate (deha) in rats

The excretion, retention, distribution and metabolism of di-(2-ethylhexyl)adipate (DEHA) have been studied in the rat.After oral administration of [¹⁴C]DEHA, almost all the dose was excreted within 48 h, predominantly in the urine and as respiratory carbon dioxide. The faecal excretion was low. There was no evidence of the accumulation of radioactivity in any organs or tissues. Adipic acid (AA) was found to be the main urinary metabolite; it was also detected in the digestive tract, blood and liver.In vitro, DEHA was hydrolyzed at a significant rate by tissue preparations prepared from liver, pancreas and small intestine of the rat.These results suggest that orally administered DEHA is rapidly hydrolyzed in the body to form AA without any accumulation of mono-(2-ethylhexyl)adipate (MEHA).     

Aqueous Solubility and Daphnia magna Chronic Toxicity of Di(2-ethylhexyl) Adipate

A water solubility of 5.5 (+/-0.22) microg/L for di(2-ethylhexyl) adipate (DEHA) was measured using the slow-stir method. This value is consistent with computer estimations and over two orders of magnitude lower than that previously determined using the shake-flask method. We performed a 21-day chronic Daphnia magna limit test at an average exposure of 4.4 microg/L in laboratory diluent water to avoid insoluble test material and avoid physical entrapment. One hundred percent of the DEHA-treated organisms survived compared to 90% survival in both the controls and solvent controls. Mean neonate reproduction was 152, 137, and 148 and mean dry weight per surviving female was 0.804, 0.779, and 0.742 mg in the DEHA treatment, control, and solvent control, respectively. No adverse effects were observed.     

Peroxisome proliferation due to di (2-ethylhexyl) adipate, 2-ethylhexanol and 2-ethylhexanoic acid

The dose-response relationships for peroxisome proliferation due to Di (2-ethylhexyl) adipate (DEHA), 2-ethylhexanol (EH), 2-ethylhexanoic acid (EHA) have been investigated in rats and mice. Linear dose-response relationships were observed for induction of cyanide-insensitive palmitoyl CoA oxidation (PCO), used as a enzyme marker of peroxisome proliferation, by DEHA, EH and EHA in both species. Relative liver weights were also increased in a dose related manner. On a molar basis, DEHA was twice as potent as EH or EHA which were equipotent and PCO was stimulated to a greater extent in male mice than in rats or female mice. At doses above 8 mmol/kg/day, EH was toxic to rats (both sexes) and similarly EHA at 13.5 mmol/kg/day lead to the death of female rats. In a attempt to explain the species difference in carcinogenicity of DEHA previously reported, we also used Fischer 344 rats and B6C3F1 mice. DEHA administration (2.5 g/kg/day) to Fischer 344 rats and B6C3F1 mice lead to toxicity in female rats. Relative liver weights were increased in a dose related fashion by DEHA administration to both rats and mice, PCO but not catalase was markedly increased (up to 15 fold in male rats). Light microscopy examination indicated some glycogen loss, a dose related hypertrophy and increased eosinophilia in both rats and mice. Electron microscopy confirmed peroxisome proliferation accompanied by a marked reduction of lipid in the centrilobular hepatocytes. These data suggest EHA to be the proximate peroxisome proliferator derived from DEHA. These data indicate a higher sensitivity for Fischer 344 rats than B6C3F1 mice to hepatic peroxisome proliferation due to DEHA and ratio of PCO activity and catalase activity data suggest that more hydrogen peroxide (H₂O₂) could escape from peroxisomes in male Fischer 344 rats than B6C3F1 mice. These data obtained with B6C3F1 mice and Fischer 344 rats are not agreement with the carcinogenicity bioassays previously reported showing an incidence of hepatic tumours only in B6C3F1 mice.     

The absence of testicular atrophy and in vivo and in vitro effects on hepatocyte morphology and peroxisomal enzyme activities in male rats following the administration of several alkanols

Previous studies have shown that ethylhexanol (2-EH) and its oxidation products, but not n-hexanol, produce hepatomegaly, peroxisomal proliferation and hypotriglyceridaemia. In the present studies we have confirmed that at 1 mmol/kg doses, neither the linear nor branched chain alcohols induce testicular atrophy, hepatomegaly, peroxisome proliferation or hypolipidaemia. In vivo, neither the free alcohols nor their metabolic products seem to be responsible for the activity of the parent plasticiser. The released monoesters are probably the more potent metabolic products responsible for the hepatomegaly, peroxisomal proliferation and hypolipidaemia. This contention is supported by the in vitro hepatocyte data which demonstrate the induction of peroxisomal oxidative enzymes by MEHP whereas the alcohols were without effects.     

溶解沉淀-气相色谱法测定聚氯乙烯食品保鲜膜中增塑剂己二酸二(2-乙基)己酯(DEHA)含量

目的：研究开发了溶解沉淀前处理技术结合毛细管气相色谱法测定聚氯乙烯食品保鲜膜中己二酸二（2-乙基）己酯（DEHA）含量。方法：采用四氢呋喃作为溶剂，甲醇作为沉淀剂，可有效的将DEHA从聚氯乙烯薄膜中分离出来，然后采用非极性DB-1MS毛细管气相色谱柱进行分离，氢火焰离子化检测器检测，以气相色谱质谱进行确证。结果：DEHA在1．0～100．0mg／L范围内线性关系良好，相关系数o．999，方法回收率在87．8％-99．1％之间，相对标准偏差小于5％，检测限为0．1mg／L。结论：该方法操作简便，测定结果准确可靠，适合聚氯乙烯保鲜膜中DEHA含量的测定。     

Biomonitoring of phthalate metabolites in the Canadian population through the Canadian Health Measures Survey (2007–2009)

Human exposure to phthalates occurs through multiple sources and pathways. In the Canadian Health Measures Survey 2007–2009, 11 phthalate metabolites, namely, MMP, MEP, MnBP, MBzP, MCHP, MCPP, MEHP, MEOHP, MEHHP, MnOP, and MiNP were measured in urine samples of 6–49 year old survey respondents (n = 3236). The phthalate metabolites biomonitoring data from this nationally-representative Canadian survey are presented here. The metabolites MEP, MnBP, MBzP, MCPP, MEHP, MEOHP and MEHHP were detected in >90% of Canadians while MMP, MCHP, MnOP and MiNP were detected in <20% of the Canadian population. Step-wise regression analyses were carried out to identify important predictors of volumetric concentrations (μg/L) of the metabolites in the general population. Individual multiple regression models with covariates age, sex, creatinine, fasting status, and the interaction terms age × creatinine, age × sex and fasting status × creatinine were constructed for MEP, MnBP, MBzP, MCPP, MEHP, MEOHP and MEHHP. The least square geometric mean (LSGM) estimates for volumetric concentration (μg/L) of the metabolites derived from respective regression models were used to assess the patterns in the metabolite concentrations among population sub-groups. The results indicate that children had significantly higher urinary concentrations of MnBP, MBzP, MEHP, MEHHP, MEOHP and MCPP than adolescents and adults. Moreover, MEP, MBzP, MnBP and MEOHP concentrations in females were significantly higher than in males. We observed that fasting status significantly affects the concentrations of MEHP, MEHHP, MEOHP, and MCPP metabolites analyzed in this study. Moreover, our results indicate that the sampling time could affect the DEHP metabolite concentrations in the general Canadian population.