Because of the logistic complexity, excessive respondent burden, and high cost of conducting 24-h urine collections in a national survey, alternative strategies to monitor sodium intake at the population level need to be evaluated. We conducted a calibration study to assess the ability to characterize sodium intake from timed-spot urine samples calibrated to a 24-h urine collection. In this report, we described the overall design and basic results of the study. Adults aged 18-39 y were recruited to collect urine for a 24-h period, placing each void in a separate container. Four timed-spot specimens (morning, afternoon, evening, and overnight) and the 24-h collection were analyzed for sodium, potassium, chloride, creatinine, and iodine. Of 481 eligible persons, 407 (54% female, 48% black) completed a 24-h urine collection. A subsample (n = 133) collected a second 24-h urine 4-11 d later. Mean sodium excretion was 3.54 ± 1.51 g/d for males and 3.09 ± 1.26 g/d for females. Sensitivity analysis excluding those who did not meet the expected creatinine excretion criterion showed the same results. Day-to-day variability for sodium, potassium, chloride, and iodine was observed among those collecting two 24-h urine samples (CV = 16-29% for 24-h urine samples and 21-41% for timed-spot specimens). Among all race-gender groups, overnight specimens had larger volumes (P < 0.01) and lower sodium (P < 0.01 to P = 0.26), potassium (P < 0.01), and chloride (P < 0.01) concentrations compared with other timed-spot urine samples, although the differences were not always significant. Urine creatinine and iodine concentrations did not differ by the timing of collection. The observed day-to-day and diurnal variations in sodium excretion illustrate the importance of accounting for these factors when developing calibration equations from this study.

We developed and tested calibration equations from spot urine specimens to estimate the distribution of usual 24h sodium excretion (24UNa). A convenience sample of 407 adults, 18‐39 y, (54% female, 48% black) collected each void in a separate container for 24h; 133 collected a second 24h urine 4‐11 d later. We selected 4 timed voids (morning [M], afternoon [A], evening [E], overnight [O]) from each 24h collection. Participants were randomly assigned to test (n=247) or validation (n=160) groups. Total sodium excreted in each of the 4 one‐spot and 6 combined two‐spot (e.g., M+A) urines from the test groups were used with covariates to develop sex‐specific equations for predicting 24UNa using Fuller’s error‐in‐the‐equation measurement error model. Equations applied to the validation data were used to estimate usual 24UNa distributions with the Iowa State University method. Mean bias in predicting the median of 24UNa with one‐spot urines ranged from ‐69 to 1617 mg for men and ‐72 to ‐9 mg for women, and with two‐spot urines from ‐124 to 115 mg and ‐50 to 9 mg, respectively. Mean bias in predicting percentiles (5th, 25th, 50th, 75th, and 95th) did not differ from 0 (p=0.06‐0.90) for men or women using an O void or combined E+O urine. Our method to estimate population distribution of 24UNa, which uses timed‐spot urine specimens and accounts for day‐to‐day variation and covariance between measurement errors, merits further investigation.

P78 Epidemiologic studies suggest that dietary vitamin E intake is inversely related to the risk of coronary heart disease (CHD). We examined the relationship between dietary intake of vitamin E and incidence of and mortality from CHD and cardiovascular disease (CVD) in 9,766 men and women who participated in the NHANES I Epidemiologic Follow-up Study and were free of CVD at their baseline examination. A 24-hour dietary recall was conducted at the baseline examination and nutrient intakes were recalculated using ESHA Food Processor software. Other important risk factors for CVD including age, sex, race, serum cholesterol, blood pressure, body mass index, history of diabetes, education, physical activity, cigarette smoking, and alcohol consumption were also measured at baseline. Those risk factors and dietary intake of saturated fat and total energy were used for adjustment in multivariate analyses. Incidence and mortality data for CHD and CVD were obtained from medical records and death certificates. Cox proportional hazard models were used to examine the relationship between dietary vitamin E intake and the incidence of and mortality from CHD and CVD. Over an average of 19 years of follow-up, 1,845 incident cases of CHD (669 fatal) and 3,760 incident cases of CVD (1,197 fatal) were documented. The adjusted relative risk (RR) was 0.89 (95% confidence interval [CI], 0.77-1.02, p=0.03 for trend) for incident CHD events, 0.69 (95% CI: 0.55−.86, p=0.001 for trend) for fatal CHD events, and 0.85 (95% CI: 0.70-1.02, p=0.03 for trend) for fatal CVD events among those in the highest quartile of dietary vitamin E intake (median, 17.5 mg/d) compared with those in the lowest quartile (median, 3.0 mg/d). These findings support the hypothesis that increasing vitamin E intake may be an important element of dietary approaches to reducing the incidence of and mortality from CHD in the US population.