1987; Nilsson et al. 1991). In spite of the long

follow-up times, they did still not allow accurate estimates of the slow phase. Thus, we choose to use the better value obtained in our earlier study. The present P–Pbs are much higher than those in Swedes with no particular exposure (0.1–0.3 μg/L (Schütz et al. 1996; Bergdahl et al. 1999), and remained so long after end of exposure. Therefore, we did not subtract a level in Swedish subjects without excessive exposure. The method for determination of P–Pb with ICP-MS has been further developed. Hence, at our laboratory, the limit of detection is now 0.02 μg/L and the precision 6%. Hence, it is possible to use P–Pb as a biomarker in environmental health. The number of cases is small, in particular we had only three cases with valid Repotrectinib solubility dmso AR-13324 datasheet information on long-term B-Hb, which must be taken into consideration when drawing conclusions. In addition, the time of exposure and the total amount of Pb absorbed varied between the individuals; in particular, Case 5 differed. Hence, the body burden (mainly the skeletal content) of Pb differed, which will affect the elimination pattern after end of exposure (Nilsson et al. 1991). This

was click here accounted for by the use of a two-component elimination model on an individual basis. The relationship between the initial levels of the two components will vary depending upon the bone pool versus Adenylyl cyclase recent exposure. The pattern of P–Pb fits better with exposure data than B–Pb, which may be because it better reflects uptake and body burden, especially at these high uptakes. Only after careful comparison of the patterns did we merge the information into combined conclusions. The T

1/2 for P–Pb of about 1 month is much longer than that reported after intravenous injection of Pb salt (Campbell et al. 1984). The present T 1/2s for B–Pb are longer than previously reported (Schütz and Skerfving 1976; Rabinowitz et al. 1976; Schütz et al. 1987). This is certainly because the present cases had B-Pbs much higher than in the earlier studies. Thus, our subjects initially had anaemia, with an attenuation of the rate of B–Pb decline when the effect on the blood cell formation and survival decreases as the body burden decays. Further – and more important – the curvilinear relationship between B–Pb and P–Pb, at the initial decrease of the body burden, will not be reflected in a simultaneous decay of B–Pb. Hence, our T 1/2s of B-Pbs are fully compatible with both the earlier reports on B–Pb and our T 1/2s for P–Pb. Also, the non-linear B–Pb/P–Pb relationship means that the B–Pb/P–Pb ratio will differ between individuals and over time. In spite of the time to diagnosis being long in some of the cases, the modelling resulted in estimates of both the B–Pb and the P–Pb content at t = 0, which marked the actual end of exposure.