Variation in drug elimination may explain why some patients in this clinical trial experience severe toxicities or inadequate antitumour effects.
Finally, we analyse model parameter values estimated from each study area in order to investigate the factors that underlie the observed between-community variation in these elimination thresholds.
It is generally assumed a single measurement of POPs in the body reflects lifetime exposure, although there is variation in the elimination rate between individuals, caused by, for example, age, lactation, and changes in body weight.
On the other hand, inter-patient variations in AI elimination can cause highly variable plasma concentrations despite regular drug intake.
However, the equation proposed by Flesch-Janys et al. (1996) may be problematic for ages > 60 years because very small variations in the elimination rate could lead to substantial divergence in half-life length, as observed in the case of 1,2,3,7,8-PeCDD.
These findings are particularly relevant for epidemiological studies of health risks associated with low environmental exposures to Cd. Observations in these studies based on U-Cd would be substantiated by the use of cumulative intake indicators that are unlikely to be confounded by recent Cd exposure and physiological variations in renal elimination of the metal.
There is no evidence for a gender difference in exposure, so variation in metabolism or elimination due to body fat or hormone-related factors may explain this finding.
The interindividual variation in the estimated elimination rates for each of the congeners generally encompassed an approximately 2-fold increase in apparent half-life from the 25th to the 75th percentile.
Less is known about the variation in other critical hepatic elimination processes such as active biliary excretion by multidrug resistance gene 1 (multidrugltidresistance-associatedated protein 2 (MRP2) and the other ATP binding cassette (ABC) family of efflux pumps, although some polymorphisms have been identified (Tanabe et al, 2001).
Overexpression, deletions, epigenetic modifications, or single-nucleotide polymorphisms in the mature miRNA may result in elimination or variations in the binding affinity to the target mRNA, triggering gene regulation imbalances in both normal and disease conditions [ 57].
