Exhalation rate steady-state

One, or actually two questions must be raised in connection with the exhalation behaviour exemplified in Figure 2. For how long will the exhalation decrease and what is the final steady-state exhalation value The latter question is the easier one, as the quotient free exhalation rate, Eq, to final steady-state exhalation with the can closed, E, is (cf. Figure 2 for the notation) ... 

For a thin sample (d<0.5L), like that in Figure 2, the quotient is equal to (1+a)/ a where a equals h/(pd), the outer to inner volume ratio. Applying Equation 2 to our case in Figure 2 the steady-state exhalation rate is simply half of the free exhalation rate. 

Table I. The 95% gradient reshaping times (see text) for different combinations of sample thickness, d, outer volume height, h, and diffusion length, L. The quotient free exhalation rate, Eq, and the final steady-state exhalation rate, E, is also given.

If we choose a much larger than 1 (thin samples d<0.5L) or h pL (thick samples d>>L), the final steady-state exhalation deviates very little from the free exhalation rate and we do not need to know the reshaping time or use Equation 2 for corrections. An air grab sample taken at any time (and corrected for radioactive decay if necessary) after closure, will yield the free exhalation rate to a good approximation, provided that the can is perfectly radon-tight. 

Figure 6 displays exhalation rate curves versus time for the sample in Figure 2, with the leakage factory as the variable parameter. Large leaks make the final steady-state exhalation rate deviate less from the free exhalation rate, in accordance with Equation 4. It must be remembered, however, that the radon activity accumulating in the outer volume is dependent on y, the exhalation rate is only the strength of the radon source feeding this volume. 

The radon emanation and the ventilation rate of a room can be derived from the increase of the radon concentration by the radon exhalation and from the steady state condition between exhalation and air exchange with the free atmosphere. In Fig. 2 the variation of the radon concentration as function of time is shown measured in two houses with different radon emanations and ventilation rates. 

Although there are many cases of human overexposure to carbon tetrachloride vapor, there are few quantitative studies of pulmonary absorption of carbon tetrachloride in humans. Based on the difference in carbon tetrachloride concentration in inhaled and exhaled air, absorption across the lung was estimated to be about 60% in humans (Lehmann and Schmidt-Kehl 1936). In animals, monkeys exposed to 50 ppm absorbed an average of 30.4% of the total amount of carbon tetrachloride inhaled, at an average absorption rate of 0.022 mg carbon tetrachloride/kg/minute (McCollister et al. 1951). The concentration of carbon tetrachloride in the blood increased steadily, but did not reach a steady-state within 344 minutes of exposure. 

Many commonly measured pharmacokinetic values can be used as biomarkers of exposure. Examples include parent compound or metabolites in exhaled breath, blood, or urine and macromolecular adducts or their degradation products that appear in urine. To make quantitative assessments of the relationship of such markers to prior exposures, it is necessary to determine the rate of formation and removal (clearance) of the marker. From this information it is possible to predict the steady-state concentrations of the marker following various exposure scenarios. In addition, with information on the rate of formation and removal of a marker and knowledge of the factors that influence those rates (such as gender, dose, repeated exposures, route of exposure, rate of exposure), a mathematical model that describes the concentration of the marker under different exposure conditions can be developed. While the concentration of the marker cannot be used to identify a unique exposure scenario, the marker can indicate the types of exposure regimens that would produce the measured level of the biomarker. 

For efficient transport of relatively insoluble CO2 from the tissues where it is formed to the lungs where it must be exhaled, the buffers of the blood convert CO2 to the very soluble anionic form HCOJ (bicarbonate ion). The principal buffers in blood are bicarbonate-carbonic acid in plasma, hemoglobin in red blood cells, and protein functional groups in both. The normal balance between rates of elimination and production of CO2 yields a steady-state concentration CO2 in the body fluids and a relatively constant pH. 

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