The two samples (City of Augsburg, Greater Augsburg) differed significantly in a variety of individual subjects' risk factors and mean exposures, and with respect to methodological aspects (noise assessment).
This suggests that high mean exposures and high peak levels may drive cytogenetic responses if they are considered to be FA induced.
In contrast, our kriging-based approach estimated daily mean exposures and SEs at geocoded addresses of participants and their examination sites across the contiguous United States that can be readily integrated over time with little influence of missing data.
We first analyzed published data to calculate mean exposure concentrations and estimated age-dependent inhalation intakes.
The primary endpoints include independent associations between integrated 5-day mean exposure to PM2.5 and BC and homeostasis model assessment of insulin resistance (HOMA-IR) measures, 24-hour mean diastolic and mean arterial pressure and endothelial-dependent vasodilatation.
AF and AN estimates for exposures > 0.1, 0.2, 0.3 or 0.4 μT were calculated for the arithmetic mean and geometric mean exposure distributions, before and after making the 50% exposure reduction in the United States (Table 4).
The mean exposure of olmesartan and candesartan users was 126.1 and 122.8 days, respectively.
Different models are computed with different exposure variables: time since first exposure, total cumulative exposure, duration of exposure and mean exposure, that is the total cumulative exposure divided by the duration of exposure.
For example, according to the model including only time since first exposure and mean exposure, the yearly incidence increases from 0.8%100 years after the onset of exposure to 2.4%300 years after exposure onset for a mean exposure of 1 fibre/ml.
Mean exposure to UFPs and CO were approximately 20 30% (p<0.01) lower at the sidewalk and 40 50% lower at the path, than at the road (p<0.01).
