Background Few reference equations exist for healthy adults of various races for pulmonary diffusing capacity for nitric oxide (DLNO). The purpose of this study was to collect pilot data to demonstrate that race-specific reference equations are needed for DLNO. Methods African Americans (blacks) were chosen as the comparative racial group. In 2016, a total of 59 healthy black subjects (27 males and 32 females) were recruited to perform a full battery of pulmonary function tests. In the development of DLNO reference equations, a white reference sample (randomly drawn from a population) matched to the black sample for sex, age, and height was used. Multiple linear regression equations for DLNO, alveolar volume (VA), and pulmonary diffusing capacity for carbon monoxide (DLCO) using a 5–6 s breath-hold were developed. Results Our models demonstrated that sex, age2, race, and height explained 71% of the variance in DLNO and DLCO, with race accounting for approximately 5–10% of the total variance. After normalizing for sex, age2, and height, blacks had a 12.4 and 3.9 mL/min/mmHg lower DLNO and DLCO, respectively, compared to whites. The lower diffusing capacity values in blacks are due, in part, to their 0.6 L lower VA (controlling for sex and height). Conclusion The results of this pilot data reveal small but important and statistically significant racial differences in DLNO and DLCO in adults. Future reference equations should account for racial differences. If these differences are not accounted for, then the risk of falsely diagnosing lung disease increase in blacks when using reference equations for whites.

The risk of cardiovascular disease (CVD) including hypertension is higher in South Asians (SAs) than White Europeans (WEs). But, whether disturbances in autonomic control of the cardiovascular system are present in early adulthood in SAs has not been tested. Thus, we performed studies on young 20 WEs and 21 SAs aged (21.9±0.36, 20.7±0.41 respectively, equal numbers of men and women in each group) in whom arterial blood pressure (ABP), electrocardiogram (ECG), heart rate (HR) and respiration were recorded at rest, during mental stress (3 min Colour Stroop test) and during 5 min slow breathing (6 breaths/min). Stroke volume (SV), cardiac output (CO), and total peripheral resistance (TPR) were computed from the pulse contour. Baroreflex sensitivity (BRS) was calculated by the sequence method as change in R‐R interval evoked by spontaneous up and down sequences in systolic pressure (SP) at rest and during mental stress and as the relationship between R‐R interval and the fall in SP evoked by standing from a squat before and at 0, 3, 6 min following the stress test. HRV was computed in time‐domain during mental stress and slow breathing. Comparisons within and between WEs and SAs were done by paired and un‐paired t‐tests respectively. At rest, WEs and SAs had similar mean ABP (mABP, 86.9±1.42 vs 87.1±1.77mmHg), HR (71.1±2.45 vs 76.2±3.56 beats/min), CO (4.8±0.21 vs 5.2±0.21L/min), SV (76.5±3.86 vs 81.5±2.97ml), TPR (1.14±0.06 vs 1.01±0.04 resistance units), and BRS (up‐sequence: 1.2±0.05, down‐sequence: 1.2±0.05 vs 1.0±0.09 and 1.2±0.09ms/mmHg). Further, mental stress evoked similar increases in mABP and HR in WEs and SAs but was accompanied by an increase CO in WEs and by an increase in TPR in SAs. Concomitantly, vagal indices of HRV were depressed during mental stress in SAs only (RMSSD: 66.2±7.8 to56.2±11.4 and 67.6±8.7 to 50.0±6.5*ms, *: P<0.05 within WE or SAs). Further during up‐sequences in SP, BRS was depressed in both SAs and WEs during mental stress, but during down‐sequences, BRS was depressed in WE only (to 0.59±0.10 vs 0.96±0.08*ms/mmHg). Also, following mental stress, BRS during squat to stand, an index of vagosympathetic activity, was depressed in WEs only (0.5±0.04 at rest to 0.3±0.04* vs 0.5±0.06 to 0.5±0.06ms/mmHg). On the other hand, slow breathing, tended to decrease ABP in both WEs and SAs (82.1±1.8 to 79.2±2.1mmHg: P<0.05; 79.4±2.0 to 77.4±2.0mmHg: P=0.09 respectively) and increased vagal indices of HRV in both WEs and SAs (66.3±8.6 to 86.0±13.2*ms; 67.6±8.7 to 86.48.8*ms). These results suggest that during and after mental stress, young normotensive SAs show greater sympathetic vasoconstriction than WEs, and attenuated respiratory modulation of HR, while their ability to evoke baroreflex tachycardia by vagal inhibition and sympathetic activation is preserved relative to young WEs. Such disturbances in would be expected to increase the risk of future CVD and hypertension in SAs, particularly in those with high levels of daily stress. The finding that slow breathing increased vagal activity in you...