Document MG793DGQV8B2p5rgk4pmG9rmV

Conclusions 1. P C B s , PCDDs and PCDFs prevail globaLly. They are persistent and have a cumulative tendency in biological systems. Contaminated food is likely to be the main source .i ) p ur ^ E x p o s u r e s higher than the av er a ge r.ay be caused by toxic wastes and th-e-w45- incineration, certain industries such as metal industries, car exhaust, various electrical n.( r * .app-l ianctts and production and use of c h 1o r oph e no 1s and phenoxy herbicides. Exposures may occur occupationally and, in the general population, also including women of . i , w* CJ t j , . -f-er-ti-l-e age. ttLt, 2. Nine major congeners of PCDDs and PCDFs are found ffleesurable in human milk fat at c o nc en tra ti ons of a few . up to more than 1000 ppt (ng/kg). Toxicity eq ui valent factors have been estimated in order to assess the s i g n i f i cance of exposure to the mixture of these compounds as an interim procedure until more accurate methods have been developed. 3. More than 70 PCB congeners have been identified in human milk fat and adipose tissue at total average concentr ations of 1 ppm (mg/kg). Toxic equivalent factors cannot be applied to such mixtures. 4. The daily intakes of PCBs in human milk are estimated to be on average in the order of 4.2 ug/kg bw/d giving a total dose for 6 monttts of about 750 ug/kg/bw. The average intake for PCDDs and PCDFs expressed as TCDD equivalent is 70 pg/kg/bw/d which makes 12.6 ng/kg bw during a 6-raonth nursing period. i i*