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Low-level cadmium exposure has adverse effects on chronic kidney disease (CKD); however, the risk factors for elevated blood cadmium levels (BCLs) have not been studied in CKD. We conducted a cross-sectional investigation in 200 CKD patients and stratified them by the tertiles of BCL to compare their demographic, environmental, and biochemical data. The factors associated with BCL were identified, and their effects were examined in subgroups. In the analyses, female sex, smoking, and CKD stage 5D were associated with high BCL, and statin was inversely correlated with BCL (odds ratio [95% confidence interval, CI], 6.858 [2.381-19.746], p < 0.001, 11.719 [2.843-48.296], p = 0.001, 30.333 [2.252-408.520], p = 0.010, and 0.326 [0.122-0.873], p = 0.026; deviations of BCL [nmol/L, 95% CI], 2.66 [1.33-4.00], p < 0.001, 3.68 [1.81-5.56], p < 0.001, 3.38 [0.95-5.82], p = 0.007, and -2.07 [-3.35--0.78], p = 0.002). These factors were also independently correlated with BCL in subgroups, including non-dialysis CKD, hypertensive patients, non-smokers, and male patients. In conclusion, female sex, smoking, and CKD stage 5D were the major risk factors for elevated BCL; additionally, statins were negatively associated with BCL in CKD.

Pneumonia, one of the important causes of death in children, may be induced or aggravated by particulate matter (PM). Limited research has examined the association between PM and its constituents and pediatric pneumonia-related emergency department (ED) visits. Measurements of PM 2.5 , PM 10 , and four PM 2.5 constituents, including elemental carbon (EC), organic carbon (OC), nitrate, and sulfate, were extracted from 2007 to 2010 from one core station and two satellite stations in Kaohsiung City, Taiwan. Furthermore, the medical records of patients under 17 years old who had visited the ED in a medical center and had a diagnosis of pneumonia were collected. We used a time-stratified, case-crossover study design to estimate the effect of PM. The single-pollutant model demonstrated interquartile range increase in PM 2.5 , PM 10 , nitrate, OC, and EC on lag 3, which increased the risk of pediatric pneumonia by 18.2% (95% confidence interval (Cl), 8.8-28.4%), 13.1% (95% CI, 5.1-21.7%), 29.7% (95% CI, 16.4-44.5%), 16.8% (95% CI, 4.6-30.4%), and 14.4% (95% Cl, 6.5-22.9%), respectively. After PM 2.5 , PM 10 , and OC were adjusted for, nitrate and EC remained significant in two-pollutant models. Subgroup analyses revealed that nitrate had a greater effect on children during the warm season (April to September, interaction p = 0.035). In conclusion, pediatric pneumonia ED visit was related to PM 2.5 and its constituents. Moreover, PM 2.5 constituents, nitrate and EC, were more closely associated with ED visits for pediatric pneumonia, and children seemed to be more susceptible to nitrate during the warm season.

Background: PM 2.5 exposure is associated with pulmonary and airway inflammation, and the health impact might vary by PM 2.5 constitutes. This study evaluated the effects of increased short-term exposure to PM 2.5 constituents on chronic obstructive pulmonary disease (COPD)-related emergency department (ED) visits and determined the susceptible groups., Methods: This retrospective observational study performed in a medical center from 2007 to 2010, and enrolled non-trauma patients aged >20 years who visited the emergency department (ED) and were diagnosed as COPD. Concentrations of PM 2.5 , PM 10 , and the four PM 2.5 components, including organic carbon (OC), elemental carbon (EC), nitrate (NO 3 - ), and sulfate (SO 4 2- ), were collected by three PM supersites in Kaohsiung City. We used an alternative design of the Poisson time series regression models called a time-stratified and case-crossover design to analyze the data., Results: Per interquartile range (IQR) increment in PM 2.5 level on lag 2 were associated with increments of 6.6% (95% confidence interval (CI), 0.5-13.0%) in risk of COPD exacerbation. An IQR increase in elemental carbon (EC) was significantly associated with an increment of 3.0% (95% CI, 0.1-5.9%) in risk of COPD exacerbation on lag 0. Meanwhile, an IQR increase in sulfate, nitrate, and OC levels was not significantly associated with COPD. Patients were more sensitive to the harmful effects of EC on COPD during the warm season (interaction p = 0.019). The risk of COPD exacerbation after exposure to PM 2.5 was higher in individuals who are currently smoking, with malignancy, or during cold season, but the differences did not achieve statistical significance., Conclusion: PM 2.5 and EC may play an important role in COPD events in Kaohsiung, Taiwan. Patients were more susceptible to the adverse effects of EC on COPD on warm days.

The links of air pollutants to health hazards have been revealed in literature and inflammation responses might play key roles in the processes of diseases. WBC count is one of the indexes of inflammation, however the l iterature reveals inconsistent opinions on the relationship between WBC counts and exposure to air pollutants. The goal of this population-based observational study was to examine the associations between multiple air pollutants and WBC counts. This study recruited community subjects from Kaohsiung city. WBC count, demographic and health hazard habit data were collected. Meanwhile, air pollutants data (SO 2 , NO 2 , CO, PM 10 , and O 3 ) were also obtained. Both datasets were merged for statistical analysis. Single- and multiple-pollutants models were adopted for the analysis. A total of 10,140 adults (43.2% males; age range, 33~86 years old) were recruited. Effects of short-term ambient concentrations (within one week) of CO could increase counts of WBC, neutrophils, monocytes, and lymphocytes. However, SO 2 could decrease counts of WBC, neutrophils, and monocytes. Gender, BMI, and smoking could also contribute to WBC count increases, though their effects are minor when compared to CO. Air pollutants, particularly SO 2 , NO 2 and CO, may thus be related to alterations of WBC counts, and this would imply air pollution has an impact on human systematic inflammation.

Background: Air pollution exposure is associated with greater risk for cardiovascular events. This study aims to examine the effects of increased exposure to short-term air pollutants on ST-segment elevation myocardial infarction (STEMI) and determine the susceptible groups., Methods: Data on particulate matter PM2.5 and PM10 and other air pollutants, measured at each of the 11 air-quality monitoring stations in Kaohsiung City, were collected between 2011 and 2016. The medical records of non-trauma adult (>17 years) patients who had visited the emergency department (ED) with a typical electrocardiogram change of STEMI were extracted. A time-stratified and case-crossover study design was used to examine the relationship between air pollutants and daily ED visits for STEMI., Results: An interquartile range increment in PM2.5 on lag 0 was associated with an increment of 25.5% (95% confidence interval, 2.6%-53.4%) in the risk of STEMI ED visits. Men and persons with ≥3 risk factors (male sex, age, hypertension, diabetes, current smoker, dyslipidemia, history of myocardial infarction, and high body mass index) for myocardial infarction (MI) were more sensitive to the hazardous effects of PM2.5 (interaction: p = 0.039 and p = 0.018, respectively). The associations between PM10, NO2, and O3 and STEMI did not achieve statistical significance., Conclusion: PM2.5 may play an important role in STEMI events on the day of exposure in Kaohsiung. Men and persons with ≥3 risk factors of MI are more susceptible to the adverse effects of PM2.5 on STEMI.