An accurate assessment of pollutants’ exposure and precise evaluation of the clinical outcomes pose two major challenges to the contemporary environmental health research. The common methods for exposure assessment are based on residential addresses and are prone to many biases. Pollution levels are defined based on monitoring stations that are sparsely distributed and frequently distanced far from residential addresses. In addition, the degree of an association between outdoor and indoor air pollution levels is not fully elucidated, making the exposure assessment all the more inaccurate. Clinical outcomes’ assessment, on the other hand, mostly relies on the access to medical records from hospital admissions and outpatients’ visits in clinics. This method differentiates by health care seeking behavior and is therefore, problematic in evaluation of an onset, duration, and severity of an outcome. In the current paper, we review a number of novel solutions aimed to mitigate the aforementioned biases. First, a hybrid satellite-based modeling approach provides daily continuous spatiotemporal estimations with improved spatial resolution of 1 × 1 km2 and 200 × 200 m2 grid, and thus allows a more accurate exposure assessment. Utilizing low-cost air pollution sensors allowing a direct measurement of indoor air pollution levels can further validate these models. Furthermore, the real temporal-spatial activity can be assessed by GPS tracking devices within the individuals’ smartphones. A widespread use of smart devices can help with obtaining objective measurements of some of the clinical outcomes such as vital signs and glucose levels. Finally, human biomonitoring can be efficiently done at a population level, providing accurate estimates of in-vivo absorbed pollutants and allowing for the evaluation of body responses, by biomarkers examination. We suggest that the adoption of these novel methods will change the research paradigm heavily relying on ecological methodology and support development of the new clinical practices preventing adverse environmental effects on human health.
One of the most clinically important effects following the administration of packed cell transfusion (PCT) is hyperkalemia, which can cause severe life-threatening cardiac arrhythmias. This retrospective population-based cohort study included adults hospitalized between January 2007 and December 2019 in a general intensive care unit for 24 h or more, with normal levels of serum potassium on admission. We assessed changes in serum potassium levels after administration of one unit of packed cells and sought to identify clinical parameters that may affect these changes. We applied adjusted linear mixed models to assess changes in serum potassium. The mean increase in serum potassium was 0.09 mEq/L (C.U 0.04–0.14, p-value < 0.001) among the 366 patients who were treated with a single PCT compared to those not treated with PCT. Increased serum potassium levels were also found in patients who required mechanical ventilation, and to a lesser degree in those treated with vasopressors. Hypertension, the occurrence of a cerebrovascular accident, and increased creatinine levels were all associated with reduced serum potassium levels. Due to the small rise in serum potassium levels following PCT, we do not suggest any particular follow-up measures for critically ill patients who receive PCT.
Hypokalemia is common among critically ill patients. Parenteral correction of hyperkalemia depends on dosages and patient characteristics. Our aims were to assess changes in potassium levels following parenteral administration, and to derive a formula for predicting rises in serum potassium based on patient characteristics. We conducted a population-based retrospective cohort study of adults hospitalized in a general intensive care unit for 24 h or more between December 2006 and December 2017, with hypokalemia. The primary exposures were absolute cumulative intravenous doses of 20, 40, 60 or 80 mEq potassium supplement. Adjusted linear mixed models were used to estimate changes in serum potassium. Of 683 patients, 422 had mild and 261 moderate hypokalemia (serum potassium 3.0–3.5 mEq/L and 2.5–2.99 mEq, respectively). Following doses of 20–80 mEq potassium, serum potassium levels rose by a mean 0.27 (±0.4) mEq/L and 0.45 (±0.54) mEq/L in patients with mild and moderate hypokalemia, respectively. Changes were associated with creatinine level, and the use of mechanical ventilation and vasopressors. Among critically ill patients with mild to moderate hypokalemia, increases in serum potassium after intravenous potassium supplement are influenced by several clinical parameters. We generated a formula to predict the expected rise in serum potassium based on clinical parameters.
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