The predictive ability of GOLD 2011 did not differ significantly from GOLD 2007 in terms of hospitalizations and mortality.

RationaleData on the change in diffusion capacity of the lung for carbon monoxide (DLCO) over time are limited. We aimed to examine change in DLCO (ΔDLCO) over a 9-year period and its predictors.MethodsA Norwegian community sample comprising 1,152 subjects aged 18–73 years was examined in 1987 and 1988. Of the 1,109 subjects still alive, 830 (75%) were re-examined in 1996/97. DLCO was measured with the single breath-holding technique. Covariables recorded at baseline included sex, age, height, weight, smoking status, pack years, occupational exposure, educational level, and spirometry. Generalized estimating equations analyses were performed to examine relations between ΔDLCO and the covariables.ResultsAt baseline, mean [standard deviation (SD)] DLCO was 10.8 (2.4) and 7.8 (1.6) mmol·min−1·kPa−1 in men and women, respectively. Mean (SD) ΔDLCO was −0.24 (1.31) mmol·min−1·kPa−1. ΔDLCO was negatively related to baseline age, DLCO, current smoking, and pack years, and positively related to forced expiratory volume in 1 second (FEV1) and weight. Sex, occupational exposure, and educational level were not related to ΔDLCO.ConclusionsIn a community sample, more rapid decline in DLCO during 9 years of observation time was related to higher age, baseline current smoking, more pack years, larger weight, and lower FEV1.

Pulmonary diffusion capacity for carbon monoxide (DL(CO)) is reduced by approximately 10% 1-6 h after maximal exercise. The mechanisms may be interstitial alveolar oedema and reduced pulmonary capillary blood volume. It was hypothesized that thermal stress following exercise contributes to the reduction in DL(CO), and that skin cooling would attenuate the postexercise reduction in DL(CO). Cutaneous vascular conductance (CVC), mean surface temperature (MST), rectal temperature and DL(CO) were measured before and 90 min after maximal incremental cycle exercise. Thereafter, the subjects were exposed to cold air without eliciting shivering one day and another day served as control. The measurements were repeated 120 min after exercise. Twelve healthy subjects (six male) aged 20-27 years were studied. DL(CO) was reduced by 7.1% (SD = 6.3%, P = 0.003) and 7.6% (SD = 5.3%, P<0.001) 90 and 120 min after exercise in the control experiment. It was reduced by 5.6% (SD = 5.5%, P = 0.014) 90 min after exercise and remained reduced by 6.1% (SD = 6.1%, P = 0.012) after cooling despite a significant reduction in CVC and in MST from 31.9 (SD = 0.6) degrees C to 27.4 (SD = 1.9) degrees C. We conclude that the postexercise reduction in DL(CO) is present when thermal status is restored after exercise, and that it is not influenced by further skin surface cooling.

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