Harmonizing analytical chemistry and clinical epidemiology for human biomonitoring studies. A case-study of plastic product chemicals in urine.

There is an interdisciplinary interface between analytical chemistry and epidemiology studies with respect to the design, execution, and analysis of environmental epidemiology cohorts and studies. Extracting meaningful results linking chemical exposure to human health outcomes begins at study design and spans the entire workflow. Here we discuss analytical experimental design from an exposure science perspective, and propose a reporting checklist for the design of human biomonitoring studies. We explain key analytical chemistry concepts of blanks and limits of reporting and present a case series of plastic product chemical exposure in prenatal urine specimens from the Barwon Infant Study.

Pulse transit time measured from the ECG: an unreliable marker of beat-to-beat blood pressure.

The arterial pulse-wave transit time can be measured between the ECG R-wave and the finger pulse (rPTT), and has been shown previously to have a linear correlation with blood pressure (BP). We hypothesized that the relationship between rPTT, preejection period (PEP; the R-wave/mechanical cardiac delay), and BP would vary with different vasoactive drugs. Twelve healthy men (mean age 22 yr) were studied. Beat-to-beat measurements were made of rPTT (using ECG and photoplethysmograph finger probe), intra-arterial radial pressure, PEP (using cardiac bioimpedance), and transit time minus PEP (pPTT). Four drugs (glyceryl trinitrate, angiotensin II, norepinephrine, salbutamol) were administered intravenously over 15 min, with stepped dosage increase every 5 min and a 25-min saline washout between agents. All subjects in all conditions had a negative linear correlation (R2 = 0.39) between rPTT and systolic BP (SBP), generally constant between different drugs, apart from four subjects who had a positive rPTT/SBP correlation with salbutamol. The 95% limits of agreement between measured and rPTT-predicted SBP were +/-17.0 mmHg. Beat-to-beat variability of rPTT showed better coherence with SBP variability than it did with heart rate variability (P < 0.001). PEP accounted for a substantial and variable proportion of rPTT (12-35%). Diastolic (DBP) and mean arterial BP (MAP) correlated poorly with rPTT (R2 = 0.02 and 0.08, respectively) but better with pPTT (rPTT corrected for PEP, R2 = 0.41 and 0.45, respectively). The 95% limits of agreement between measured and pPTT-predicted DBP were +/- 17.3 mmHg. In conclusion, the negative correlation between rPTT and SBP is generally constant, even with marked hemodynamic perturbations. However, the relationship is not reliable enough for rPTT to be used as a surrogate marker of SBP, although it may be useful in assessing BP variability. DBP and MAP cannot be predicted from rPTT without correction for PEP. The significant contribution of PEP to rPTT means that rPTT should not be used as a marker of purely vascular function.