Schmid K, Schaller K H, Angerer J, Lehnert G
Institut für Arbeits- und Sozialmedizin, Universität Erlangen-Nürnberg.
Zentralbl Hyg Umweltmed. 1994 Aug;196(2):139-52.
The suitability of the formic acid excretion in the urine as a parameter for the biological monitoring of inhalational exposure to formaldehyde is discussed controversially. We investigated persons not occupationally exposed to formaldehyde (n = 70) to determine possible influencing factors on the physiological excretion of formic acid. Following this we carried out a study on medical students (n = 30), who during an anatomical dissection course were exposed to a short but intensive inhalational exposure to formaldehyde, as well as investigations on employees of a pathological-anatomical laboratory (n = 8) in order to observe the course of the formic acid excretion in the urine during a working week with a continuous exposure to formaldehyde below or within the range of the MAK value (0.5 ppm). It was seen that the formic acid excretion in the urine with non-exposed persons is subject to considerable inter and intraindividual fluctuations (at a maximum by a factor of 30). In addition to differences in the endogenous formation of formates an important influencing factor is probably the uptake of food containing formic acid or its precursors. A value of 23 mg formic acid/g creatinine is given as the upper norm level (95th percentile) of adults. In the groups who were exposed to formaldehyde, in some cases considerably above the MAK value, we were able to detect no significant increase in the formic acid concentration in the urine. After a short but intensive exposure to formaldehyde (0.32-3.48 ppm) the formic acid concentration in the urine did not change significantly with an average formic acid concentration in the urine before exposure of 6.5 mg/g creatinine (central 50% range: 3.5-14.2 mg/g creat.) and after exposure of 6.0 mg/g creatinine (central 50% range: 4.4-10.9 mg/g creat.). There was no significant relationship between the individual change in the formic acid concentration in the urine (in mg/g creatinine) and the inhalational exposure to formaldehyde determined through personal air sampling (r = 0.079). In the course of a working week with a continuous exposure to formaldehyde (0.03-0.83 ppm) there was after relating the values to creatinine a continuous increase in the median to 22.3 mg/g creat. with a starting value of 8.7 mg/g creat. The change proved, however, for the number of cases investigated not to be significant. In particular there was no linear correlation detectable between the individual changes in the formic acid excretion in the urine and the formaldehyde concentrations in the breathing zone determined by personal air sampling.(ABSTRACT TRUNCATED AT 400 WORDS)
尿中甲酸排泄作为吸入甲醛生物监测参数的适用性存在争议。我们对未职业性接触甲醛的人群(n = 70)进行了调查,以确定可能影响甲酸生理排泄的因素。在此之后,我们对医学生(n = 30)进行了一项研究,这些医学生在解剖课程中经历了短时间但高强度的甲醛吸入暴露,还对一家病理解剖实验室的员工(n = 8)进行了调查,以观察在连续接触低于或处于MAK值(0.5 ppm)范围内的甲醛的工作周内尿中甲酸排泄的变化过程。可以看出,未接触者尿中的甲酸排泄存在相当大的个体间和个体内波动(最大相差30倍)。除了甲酸盐内源性生成的差异外,一个重要的影响因素可能是摄入含甲酸或其前体的食物。给出的成年人甲酸上限正常水平值(第95百分位数)为23毫克甲酸/克肌酐。在接触甲醛的组中,有些情况下接触水平大大高于MAK值,但我们未检测到尿中甲酸浓度有显著增加。在短时间但高强度接触甲醛(0.32 - 3.48 ppm)后,尿中甲酸浓度没有显著变化,接触前尿中甲酸平均浓度为6.5毫克/克肌酐(中间50%范围:3.5 - 14.2毫克/克肌酐),接触后为6.0毫克/克肌酐(中间50%范围:4.4 - 10.9毫克/克肌酐)。尿中甲酸浓度的个体变化(以毫克/克肌酐计)与通过个人空气采样测定的甲醛吸入暴露之间没有显著关系(r = 0.079)。在连续接触甲醛(0.03 - 0.83 ppm)的工作周过程中,将数值与肌酐相关联后,中位数从8.7毫克/克肌酐持续增加到22.3毫克/克肌酐。然而,对于所调查的病例数而言,这种变化并不显著。特别是,尿中甲酸排泄的个体变化与通过个人空气采样测定的呼吸带甲醛浓度之间未检测到线性相关性。(摘要截断于400字)