Beck H, Dross A, Mathar W
Bundesgesundheitsamt, Berlin, Germany.
Environ Health Perspect. 1994 Jan;102 Suppl 1(Suppl 1):173-85. doi: 10.1289/ehp.94102s1173.
For nonoccupationally exposed persons, the daily intake via food consumption has been calculated to be 0.35 pg/kg body weight per day for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and 2.3 pg/kg body weight per day for TCDD equivalents (TEqs). As compared to food, other sources and pathways are of minor importance. Food of animal origin contributes most, although human exposure begins with atmospheric emissions depositing these compounds on plant surfaces. In the meantime, a possible additional body burden from cardboard containers for cow's milk and coffee filters has been practically excluded. Of the 210 existing PCDDs and PCDFs, only 15 2,3,7,8-substituted isomers with a characteristic congener pattern can be found in samples of human origin. In adipose tissue and milk samples, mean levels for 2,3,7,8-TCDD of 7.2 and 3.6 pg/g fat, respectively, and of 56 (range 18-122) and 30 (range 10-72) pg TEqs/g fat, respectively, were determined. Human data revealed a dependency of polychlorinated dibenzo-p-dioxins/polychlorinated dibenzofurans (PCDD/PCDF) levels on age. In human milk, levels became reduced with the number of children born to mothers and duration of breast-feeding period. The average daily intake for a breast-fed child has been calculated to be 17 pg 2,3,7,8-TCDD/kg body weight per day and 142 pg TEqs/kg body weight per day, respectively. Levels in adipose tissue of infants, even if breast fed, were distinctly lower compared to human milk. In human milk, adipose tissue, and whole blood, PCDD/PCDF concentrations have been found to be equal on a fat-weight basis. Liver fat accumulated PCDD/PCDF with an alteration in the congener distribution pattern, whereas brain, even on a fat-weight basis, showed the lowest concentrations. Elevated or even high levels were found in occupationally exposed persons working in special chemical plants or involved in specific processes. There are limited data suggesting slightly elevated PCDD/PCDF levels are due to long-term consumption of a large share of food produced near point sources with a heavy emission or ingestion of soil or dust from such areas.
对于非职业暴露人群,经计算,通过食物摄入的2,3,7,8 - 四氯二苯并 - p - 二恶英(TCDD)的每日摄入量为0.35皮克/千克体重,TCDD当量(TEq)的每日摄入量为2.3皮克/千克体重。与食物相比,其他来源和途径的重要性较低。动物源性食物的贡献最大,尽管人类接触始于大气排放将这些化合物沉积在植物表面。与此同时,牛奶纸盒和咖啡滤纸可能带来的额外身体负担实际上已被排除。在现有的210种多氯二苯并二恶英(PCDD)和多氯二苯并呋喃(PCDF)中,在人体样本中仅能发现15种具有特征性同系物模式的2,3,7,8 - 取代异构体。在脂肪组织和牛奶样本中,2,3,7,8 - TCDD的平均含量分别为7.2和3.6皮克/克脂肪,TEq的平均含量分别为56(范围18 - 122)和30(范围10 - 72)皮克/克脂肪。人体数据显示,多氯二苯并二恶英/多氯二苯并呋喃(PCDD/PCDF)水平与年龄有关。在人乳中,PCDD/PCDF水平随着母亲生育子女的数量和哺乳期的延长而降低。经计算,母乳喂养婴儿的平均每日摄入量分别为17皮克2,3,7,8 - TCDD/千克体重和142皮克TEq/千克体重。即使是母乳喂养的婴儿,其脂肪组织中的PCDD/PCDF水平也明显低于人乳。在人乳、脂肪组织和全血中,按脂肪重量计算,PCDD/PCDF浓度相等。肝脏脂肪中积累的PCDD/PCDF具有同系物分布模式的改变,而即使按脂肪重量计算,大脑中的浓度也是最低的。在特殊化工厂工作或参与特定工艺的职业暴露人群中发现了升高甚至很高的PCDD/PCDF水平。有有限的数据表明,PCDD/PCDF水平略有升高是由于长期大量食用来自排放源附近生产的食物,或摄入这些地区的土壤或灰尘所致。