Pezzagno G, Maestri L, Fiorentino M L
Department of Preventive, Occupational and Community Medicine, University of Pavia, Italy.
Am J Ind Med. 1999 May;35(5):511-8. doi: 10.1002/(sici)1097-0274(199905)35:5<511::aid-ajim8>3.0.co;2-y.
The specificity of trans,trans-muconic acid (MA) as a biomarker of exposure to low benzene levels and the role of sorbic acid (SA) as a confounding factor were evaluated. MA, a urinary ring-opened metabolite of benzene, has been recently proposed for the biological monitoring of populations exposed to low levels of this chemical. The usual presence of MA in urine of non-occupationally exposed people is generally attributed to benzene world-wide contamination (mainly by smoking habits, urban pollution, and maybe by food contamination). However, the scientific literature reveals that the common food preservative and fungistatic agent SA is converted into MA though in trace amounts.
Urinary benzene and MA before and after administration of SA were measured in smokers and non-smokers. Benzene dissolved in urine was analyzed injecting a headspace sample in a gas-chromatografic system. Urinary MA was measured by means of a HPLC apparatus.
The mean background values of MA were about 60 mg/L (or 50 mg/g creat.); after experimental administration of SA (447 mg), the mean urinary MA concentration became more than 20 times higher. The biotransformation rates of SA into MA after ingestion of 447 mg of SA ranged from 0.05 to 0.51%. The ratio between unmetabolized benzene in the two groups of smokers and non-smokers was significantly different from the ratio between MA in the same two groups.
Other sources of MA excretion, different from benzene, influence the urinary concentration of the metabolite: only 25% of MA background values can be attributed to benzene. The urinary MA induced by 100 mg of ingested MA is 77% of that expected after an 8-hour benzene exposure to 0.5 ppm (current threshold limit value according to ACGIH). In conclusion, MA is not a sufficiently specific biomarker of low benzene exposure; a significant effect of SA ingestion is predictable.
评估反,反-粘康酸(MA)作为低苯暴露生物标志物的特异性以及山梨酸(SA)作为混杂因素的作用。MA是苯的一种尿中环开代谢物,最近被提议用于对接触低水平该化学物质人群的生物监测。非职业暴露人群尿液中通常存在MA,这一般归因于全球范围内苯的污染(主要通过吸烟习惯、城市污染以及可能的食物污染)。然而,科学文献表明,常见的食品防腐剂和抑菌剂SA虽会微量转化为MA。
在吸烟者和非吸烟者中测量给予SA前后的尿苯和MA。将溶解在尿液中的苯通过在气相色谱系统中进样顶空样品进行分析。通过高效液相色谱仪测量尿MA。
MA的平均背景值约为60mg/L(或50mg/g肌酐);在实验给予SA(447mg)后,尿MA平均浓度升高超过20倍。摄入447mg SA后SA向MA的生物转化率在0.05%至0.51%之间。两组吸烟者和非吸烟者中未代谢苯的比例与同一两组中MA的比例显著不同。
与苯不同,MA排泄的其他来源会影响该代谢物的尿浓度:只有25%的MA背景值可归因于苯。摄入100mg MA诱导的尿MA是8小时接触0.5ppm苯(根据美国政府工业卫生学家会议当前的阈限值)后预期值的77%。总之,MA不是低苯暴露的充分特异性生物标志物;摄入SA的显著影响是可预测的。