Internal exposure of nursery-school children and their parents and teachers to di(2-ethylhexyl)phtha late (DEHP)
Internal exposure of nursery-school children and their parents and teachers to di(2-ethylhexyl)phtha late (DEHP)
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DOI：
10.1078/1438-4639-00270
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发表时间：
2004-01-01
影响因子：
6
通讯作者：
Angerer, J
中科院分区：
文献类型：
--
作者：
Koch, HM;Drexler, H;Angerer, J
邻苯二甲酸二（2-乙基己基）酯是聚氯乙烯（PVC）制品的主要增塑剂。它已经在我们的环境和人群中广泛传播。DEHP被怀疑是人类内分泌干扰物的罪魁祸首。儿童可能最容易受到这些内分泌影响。在这项研究中，我们确定了幼儿园儿童（2 - 6岁）对DEHP的内部暴露，并将其与父母和老师的暴露进行了比较。在第一次晨尿中测定dehp代谢产物邻苯二甲酸单（2-乙基-5-羟基己基）酯（5OH-MEHP）、邻苯二甲酸单（2-乙基-5-氧己基）酯（5oxo-MEHP）和邻苯二甲酸单（2-乙基己基）酯（MEHP）。儿童和成人尿液中三种DEHP代谢物的总和分别为90.0和59.1马克/升（中位数，p = 0.074）。儿童的次级代谢物5OH-MEHP（中位数：49.6 vs. 32.1马克杯/升，p = 0.038）和5oxo-MEHP（中位数：33.8 vs. 19.6马克杯/升，p = 0.015）的浓度显著高于成人。成人和儿童的MEHP浓度都很低（中位数：6.6马克/升vs. 9.0马克/升）。当将儿童与成人进行比较时，肌酐调整值应更准确地反映与体重有关的剂量。儿童尿中经总肌酐调整的DEHP代谢物明显高于成人（中位数：98.8 vs 50.9马克杯/克肌酐；p < 0.0001）。这也适用于次级代谢物5OH-MEHP （55.8 vs. 28.1马克杯/克肌酐，p < 0.0001）和5o - mehp （38.3 vs. 17.2马克杯/克肌酐，p < 0.0001）的浓度。儿童和成人单酯MEHP的肌酐校正浓度非常相似（8.7 vs. 8.6马克杯/克肌酐；p = 0.908）。根据测定的三种代谢物的总和，我们估计儿童摄入的DEHP剂量（以杯/公斤体重计）大约是成人摄入剂量的两倍。无处不在的DEHP暴露途径仍不清楚。在儿童尿液中，MEHP与50H-MEHP与5oxo-MEHP的平均相对比值为1至7.1至4.9，成人为1至3.4至2.1。这可能表明儿童的氧化代谢增强。到目前为止，还没有关于DEHP氧化代谢物的生物活性和毒性的信息。由于这些是DEHP的主要代谢物，因此迫切需要这些代谢物的毒理学数据。
Di(2-ethylhcxyl)phthalate (DEHP) is the main plasticizer for polyvinyl chloride (PVC) products. It has become widely spread in our environment and among people. DEHP is suspected to be responsible for endocrine-disruptor-like effects in mankind. Children are probably most susceptible to these endocrine effects. In this study we determined the internal exposure of nursery school children (aged 2 - 6 years) to DEHP and compared it to their parents' and teachers' exposure. The DEHP-metabolites mono (2-ethyl-5-hydroxyhexyl)phthalate (5OH-MEHP), mono(2ethyl-5-oxo-hexyl)phthalate (5oxo-MEHP) and mono(2-ethylhexyl)phthalate (MEHP) were determined in first morning urine. The sum of the three DEHP metabolites in children's and in adults' urine was 90.0 and 59.1 mug/l respectively (median values; p = 0.074). Concentrations of the secondary metabolites 5OH-MEHP (median: 49.6 vs. 32.1 mug/l; p = 0.038) and 5oxo-MEHP (median: 33.8 vs. 19.6 mug/l; p = 0.015) were significantly higher in children than in adults. MEHP concentrations were low both in adults and children (median: 6.6 mug/l vs. 9.0 mug/l).Creatinine adjusted values should more accurately reflect the dose taken up with respect to body weight when comparing children with adults. Total creatinine adjusted DEHP metabolites in urine were significantly higher in children than in adults (median values: 98.8 vs. 50.9 mug/g creatinine; p < 0.0001). This also applied to the concentrations of both secondary metabolites 5OH-MEHP (55.8 vs. 28.1 mug/g creatinine; p < 0.0001) and 5oxo-MEHP (38.3 vs. 17.2 mug/g creatinine; p < 0.0001). Creatinine corrected concentrations for the monoester MEHP in children and adults were very similar (8.7 vs. 8.6 mug/g creatinine; p = 0.908). Based on the sum of the three determined metabolites we estimated the DEHP dose (in mug/kg body-weight) taken up by children to be about twice as high as the dose taken up by adults. Routes of the ubiquitous exposure to DEHP remain indistinct. In children's urine the mean relative ratios of MEHP to 50H-MEHP to 5oxo-MEHP were 1 to 7.1 to 4.9, in adults they were 1 to 3.4 to 2.1. This might indicate an enhanced oxidative metabolism in children. To date no information on the biological activity and toxicity of oxidative metabolites of DEHP is available. Since these are the major metabolites of DEHP toxicological data on these metabolites is urgently needed.