Shiftwork has been associated with elevated blood pressure (BP) and decreased heart-rate variability (HRV), factors that may increase the long-term risk of cardiovascular-related mortality and morbidity. This study explored the effect of shiftwork on dynamic changes in autonomic control of HRV (cardiac stress), systolic BP and diastolic BP, i.e., SBP and DBP (vascular stress), and recovery in the same subjects working different shifts. By studying the same subjects, the authors could reduce the effect of possible contribution of between-subject variation from genetic predisposition and environmental factors. The authors recruited 16 young female nurses working rotating shifts—day (08:00–16:00 h), evening (16:00–00:00 h), and night (00:00–08:00 h)—and 6 others working the regular day shift. Each nurse received simultaneous and repeated 48-h ambulatory electrocardiography and BP monitoring during their work day and the following off-duty day. Using a linear mixed-effect model to adjust for day shift, the results of the repeated-measurements and self-comparisons found significant shift differences in vascular stress. While working the night shift, the nurses showed significant increases in vascular stress, with increased SBP of 9.7 mm Hg. The changes of SBP and DBP seemed to peak during waking time at the same time on the day off as they did on the working day. Whereas HRV profiles usually returned to baseline level after each shift, the SBP and DBP of night-shift workers did not completely return to baseline levels the following off-duty day (p < .001). The authors concluded that although the nurses may recover from cardiac stress the first day off following a night shift, they do not completely recover from increases in vascular stress on that day. (Author correspondence: jdwang@ntu.edu.tw)
Shift work is significantly associated with BP and possibly dipper/nondipper status in young female nurses. Except for those working night shifts, BP levels returned to baseline the off-duty day after day shift. We recommend that potential influence of shift work be considered when evaluating a person's BP.
BackgroundAlthough air pollutants have been associated with cardiopulmonary mortality, their effects on the occurrence of atrial fibrillation (Afib) remain unclear. This study examined the association between ambient air pollutants and Afib occurrence.MethodsUsing a representative sample from the National Health Insurance Database of Taiwan, we applied a case–crossover study design to explore the associations between air pollutants and patients hospitalized with Afib from 2006 to 2011. The event day was when a patient was hospitalized with Afib, and the control days were the same days of the following weeks of the same month. The association between Afib occurrence and levels of ambient air pollutants (including particulate matter [PM] 2.5 PM10, NO2, SO2, and O3) was examined after adjusting for temperature and relative humidity. A two-pollutant model was used to examine the effect of the second pollutant when the first pollutant was determined to be significantly related to Afib.ResultsDuring 2006–2011, 670 patients hospitalized with the first onset of Afib were identified. The occurrence of Afib was associated with PM2.5, in which a 22% (95% confidence interval = 3–44%) increase was related to an interquartile range increase (26.2 μg/m3) on the same day and a 19% (95% confidence interval = 0–40%) increase on the second day. A two-pollutant model was applied, and the results indicated that the effect of PM2.5 was significantly associated with the occurrence of Afib. Patients aged over 65 years with DM and with hyperlipidemia were more susceptible to the effect of PM2.5.ConclusionsIn conclusion, the occurrence of Afib was associated with short-term exposure to fine particulate air pollutants in the general population.
ContextAlthough there are ample data on the respiratory effects of exposure to fire extinguisher gas, the potential hematologic effects have not been fully documented. We conducted this study to determine the possible etiologic agent(s) for a decrease in red blood cells among community residents in Taipei, Taiwan, after they were exposed to leakage of mixed fire extinguishants containing bromotrifluoromethane (CF3Br, Halon 1301), bromochlorodifluoromethane (CF2BrCl, Halon 1211), and dichlorodifluoromethane (CCl2F2, CFC-12).Case presentationWe studied 117 exposed residents who came into one hospital for physical examinations. We also selected age- and sex-matched referents for comparison from residents who came to the same hospital for health examinations. Nine months after the exposure to mixed fire extinguishants, 91 of the exposed residents came back for a second physical examination. In the first examination of the exposed residents, we found a significant reduction in red blood cell count and hemoglobin and a relationship between dose and response.DiscussionAfter excluding iron-deficiency anemia, thalassemia, and other possible agents, we suspected that the hematologic effects might have resulted from pyrolytic products of CFC-12 and Halon 1211, which may contain phosgene, among other products.Relevance to clinical practiceThe acute transient hematologic effects observed in the exposed residents were associated with the incident of leakage of mixed fire-extinguisher gases and were most likely caused by a small amount of pyrolytic products, probably phosgene. Nine months after the exposure, we found a significant improvement in the abnormalities without any specific treatment.
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