Fifteen men were exposed to 6,683 ppm C18O for 3.1 - 6.6 min. Venous and arterial blood samples were drawn at one-min intervals beginning at the start of exposure and finishing 10 min later. Simultaneously, VA was calculated from the measured values of VE and deadspace. VE was measured by integrating digitized continuous measures of inhaled and exhaled gas. All parameters of the nonlinear Coburn-Forster-Kane equation (CFKE) were measured on the individual subject except for the Haldane affinity ratio. Predictions of venous blood COHb in samples collected ca. two min after cessation of exposure were accurately predicted by the CFKE. Both venous and arterial COHb were inaccurately predicted during COHb formation, however. Venous levels were overpredicted during formation due to a delayed appearance of COHb. Individual subjects differed markedly in the delay of COHb appearance in venous blood. Arterial COHb was consistently underestimated either by the CFKE or by predictions based on venous blood samples. Thus, exposure of such organs as brain or heart to COHb can be higher than expected from previous knowledge when transient CO exposure is involved. An explanation is suggested for the observed differences between arterial and venous COHb on the basis of the regional circulation of the forearm, where both samples were taken. Because regional circulation 'Patterns are known to vary with physical training, the differences in physical training between subjects may account for the observed variation. An expanded model was derived from the Coburn-Forster-Kane equation that reflects the above hypothesis. Most of the parameter values for the expanded model were measured on :individual subjects. Literature values were used for other paramete.