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Reducing nosocomial transmission within health care facilities is important, but the number of negative-pressure airborne infection isolation rooms for SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) is limited. It is a daunting challenge to cope with a surge of suspected infectious patients in hospitals. We installed air exhaust fans on the windows to change the pressure direction within the wards rapidly. The best location for the fans was 90 cm from the floor and 90 cm from the edge of bed whether the indoor air conditioners were on or off. The noise level should be <60 dB(A) as per government regulations. General wards can be transformed into makeshift negative-pressure rooms easily and effectively within 24 hours, which is really the simple, fast, and effective way for the transformation being applied. [ABSTRACT FROM AUTHOR]

Background: Evidence on the association between long-term exposure to air pollution and cardiovascular mortality is limited in Asian populations.Methods: We conducted a cohort study on the association between fine particulate matter (PM2.5) and cardiovascular mortality using 43,227 individuals in a civil servants health service in Taiwan. Each participant was assigned an exposure level of particulate matter based on their district of residence using air pollution data collected by the Taiwan Environmental Protection Agency and with modeling using geographic information systems. The participants were followed up from 1989 to 2008 and the vital status was ascertained from death records. Cox regression models were used to adjust for confounding factors.Results: The district-level average of PM2.5 ranged from 22.8 to 32.9 μg/m(3) in the study area. After a median follow-up of 18 years, 1992 deaths from all causes including 230 cardiovascular deaths occurred. After adjustment for potential confounders, PM2.5 levels were not significantly associated with mortality from cardiovascular disease [Hazard Ratio (HR) 0.80; 95 % Confidence Interval (CI), 0.43 to 1.50 per 10 μg/m(3) increase in PM2.5] or all causes (HR 0.92; 95 % CI, 0.72 to 1.17 per 10 μg/m(3) increase in PM2.5). The results were similar when the analysis was restricted to the urban areas and when the PM2.5 measurement was changed from the period average (2000-2008) to annual average.Discussion: Our findings are different from those in prior cohort studies conducted in Asia where ambient air pollutionwas associated with an increased risk of cardiovascular mortality. The high background level of air pollutionin our study area and the small number of event cases limited the power of this study.Conclusions: In this population-based cohort study in Taiwan, we found no evidence of increased risk for all-cause or cardiovascular mortality with long-term exposure to PM2.5. [ABSTRACT FROM AUTHOR]

The biologic mechanisms involved in airway inflammatory response to air pollution are not clearly understood. The authors conducted a longitudinal study to investigate whether exposure to ambient air pollutants affected inflammatory cells and mediators from nasal lavage in schoolchildren. Study participants were 100 elementary and middle-school students in New Taipei City, Taiwan. A structured respiratory health questionnaire was administered in September 2007, followed by monthly measurement of nasal inflammation from October 2007 to November 2009. During the study period, daily concentrations of air pollutants were obtained from the Environmental Protection Administration monitoring station and the Aerosol Supersite. Mixed-effects models were applied to examine the association between air pollution and nasal inflammatory cells and mediators, including percentages of neutrophils, eosinophils, and monocytes in lavaged cells and interleukin-8. A total of 824 measurements were obtained from 100 participants over a period of 10 months. The level of particulate matter with an aerodynamic diameter of 2.5 μm or less (PM2.5) was found to be associated with percentage of neutrophils (β = 3.45%, 95% confidence interval: 0.89, 6.01) and interleukin-8 level (β = 29.98 pg/mL, 95% confidence interval: 3.26, 56.69) in the nasal lavage on the day of exposure. In this longitudinal cohort study of schoolchildren, results indicated that exposure to PM2.5 might induce nasal inflammation. [ABSTRACT FROM PUBLISHER]

Background/purpose: Psychological factors have been implicated in the etiology of idiopathic environmental illness in many studies. Few studies have ever reported psychiatric morbidity among individuals with electromagnetic hypersensitivity. We aimed to estimate the prevalence and identify the associated factors of self-reported electromagnetic field sensitivity (SREMFS) in adults of Taiwan.Methods: A total of 1251 adults selected from a nationwide Computer-Assisted Telephone Interviewing system received a telephone survey about the perception of risk from various environmental agents and their effects on health and well-being.Results: The estimated prevalence of people with SREMFS was 13.3 % (95% confidence interval: 11.2-15.3). People aged >65 years were associated with a lower risk of reporting sensitivity to electromagnetic fields, whereas people with a very poor self-reported health status, those who were unable to work, and those who had psychiatric morbidity were associated with a higher risk of having SREMFS.Conclusion: The prevalence of SREMFS in the general population of Taiwan is higher than that reported in western countries. People with psychiatric morbidity are more likely to report sensitivity to electromagnetic fields. The cross-sectional design precludes the causal inference of all identified correlates and electromagnetic field sensitivity. [ABSTRACT FROM AUTHOR]

Aims: To determine the presence of Asp13-p21-ki-ras oncoprotein and p53 oncoprotein in the plasma of vinyl chloride monomer (VCM)-workers in Taiwan. Methods: We used enhanced chemiluminescence (ECL) western blotting to detect Asp13-p21-ki-ras and ELISA to detect mutant p53 protein (p53-Ag) and anti-p53 antibodies (p53-Ab) in the plasma of VCM-exposed workers. Results: Twenty-five out of 251 (10%) VCM-workers were positive for Asp13-p21-ki-ras in plasma, but 0 out of 36 controls were positive. There were 15 out of 95 (15.8%) plasma-positives among the more highly exposed (>480 ppm-month) workers and 10 out of 156 (6.4%) plasma-positives among the lesser exposed (≤480 ppm-month). Compared to the unexposed controls, age and drinking adjusted odds ratios (95% CI) were 1.2 (0.1, 9.8) in the lower exposed workers, and 4.8 (0.8, 28) in the higher exposed workers, and there was a significant linear trend between exposure and plasma positivity (P=0.001). Thirty-three out of 251 (13.2%) VCM-workers were positive for the p53 over-expression (10% with positive p53-Ag and 2.8% with positive p53-Ab). There was a significant association between cumulative VCM exposure concentration and positive p53 expression (P=0.032) among VCM-workers after adjusting for age, hepatitis, drinking and smoking status. Conclusions: Asp13-p21-ki-ras oncoprotein and p53 over-expression (p53-Ag or p53-Ab) can be found in the plasma of VCM-workers in Taiwan, and a significant dose–response relationship exists between plasma oncoproteins expression and VCM exposure. [Copyright &y& Elsevier]

PURPOSE: To investigate the patterns of immediate seismic deaths and post-earthquake mortality changes in the disaster area after the September 21, 1999 Taiwan earthquake.METHODS: We used the data of 1,826 seismic deaths to elucidate the immediate seismic effects on mortality patterns, and to determine the association between seismic death rates and house damage among 23 townships in the disaster area. We used standardized mortality ratios (SMRs) to estimate the changes in mortality of all natural causes (ICD-9: 1–799) in the 12 months after the earthquake.RESULTS: For the 1,826 seismic deaths, two leading causes of death were asphyxiation and intracranial injury and the death rates were higher among the female and elderly population. Township-specific seismic death rates were proportional to the proportion of completely collapsed houses. SMRs decreased six months after the earthquake for all residents and female adults aged 45 years and over.CONCLUSIONS: The immediate effects of the Taiwan earthquake included a higher proportion of female and elderly seismic deaths and an association between seismic death rates and earthquake damages in the disaster area. The prolonged effect of the earthquake on mortality in the post-earthquake year was a decrease in mortality for all residents except male adults. [Copyright &y& Elsevier]

Introduction: Information on the long-term effects of different air pollutant levels on lung function is relatively lacking in Asia and still inconclusive in the world. Age differential effects of air pollution are not known., Objectives: To assess the acute and subchronic effects of ambient air pollution on lung function and compared among children of different ages., Methods: From April to May 2011, a nationwide study was conducted on schoolchildren aged 6-15 years in 44 schools of 24 districts in Taiwan. Spirograms were obtained from 1494 non-asthmatic children. Air pollution data were retrieved from air monitoring stations within one kilometre of the schools. Using three-level hierarchical linear models, individual lung function was fitted to air pollution, with adjustments for demographics, indoor exposures, outdoor activity, and districts., Results: Lung function changes per inter-quartile increase of the past two-months average levels of particulate matter <2.5 μm (PM2.5) and ozone (12 μg/m(3), 32-44 and 6.7 ppb, 32-38, respectively) were -103 and -142 ml on FVC, -86 and -131 on FEV1, and -102 and -188 ml/s on MMEF, respectively. Lag-1-day ozone exposure was associated with decreased MMEF. In children aged 6-10, PM2.5 was associated with decreased FEV1/FVC and MMEF/FVC ratios., Conclusions: In children aged 6-15 years, sub-chronic exposure to ambient PM2.5 and ozone leads to reduced lung capacity, whereas acute exposure to ozone decreases mid-expiratory flow. In children aged 6-10 years, additional airway obstructive patterns in lung function may be associated with PM2.5 exposure., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Little is known about the perceived health risks of electromagnetic fields (EMFs) and factors associated with risk perception in non-Western countries. Psychological conditions and risk perception have been postulated as factors that facilitate the attribution of health complaints to environmental factors. This study investigated people's perceived risks of EMFs and other environmental sources, as well as the relationships between risk perception, psychopathology, and the degree of self-reported sensitivity to EMFs. A total of 1,251 adults selected from a nationwide telephone interviewing system database responded to a telephone survey about the relationships between environmental sources and human health. The interview included questions assessing participants' psychiatric conditions and the presence and degree of sensitivity to EMFs. One hundred and seventy participants were self-identified as having sensitivity to EMFs, and 141 met the criteria for psychiatric conditions without EMF sensitivity. More than half of the survey respondents considered power lines and mobile phone base stations to affect people's health to a big extent. Higher sensitivity to EMFs, psychopathology, being female, being married, more years of education, and having a catastrophic illness had positive associations with perceived risks of EMF-related environmental sources as well as for all environmental sources combined. We observed no moderating effect of psychopathology on the association between degree of sensitivity to EMF and risk perception. Thus, psychopathology had influence on general people's risk perception without having influence on the relationship between people's degree of sensitivity to EMF and risk perception. The plausible explanations are discussed in the text., (© 2013 Society for Risk Analysis.)

Objectives: Studies examining the combined health effects of both have been relatively lacking. We conducted a longitudinal study to investigate whether exposure to air pollutants and fungal spores might exacerbate childhood respiratory health., Methods: Study participants were 100 elementary and middle-school students in Taipei County, Taiwan. A structured respiratory health questionnaire was administered in September 2007, followed by monthly spirometry from October 2007 to June 2008. During the study period, complete daily monitoring data for criteria air pollutants were obtained from the Environmental Protection Administration monitoring station and Aerosol Supersite. Fungal spores were measured from Sunday to Saturday in the week when lung-function measurements were made for each study month. Lung-function measurements were compared with air pollutants and fungal spores using mixed-effects models with 1-day-lag modeling., Results: The particulate matter with an aerodynamic diameter of 2.5 μm or less level 1 day before the lung function measurements was negatively associated with forced vital capacity. The fungal spore level was negatively associated with both forced expiratory vital capacity and forced expiratory volume in 1 second. O(3) level was negatively associated with forced expiratory flow at 25%, 50%, and 75% of forced vital capacity, and average expiratory flow over the middle half of forced vital capacity., Conclusions: This study suggested that exposure to particulate matter with an aerodynamic diameter of 2.5 μm or less and fungal spores might cause adverse effects on the vital capacity of schoolchildren. Exposure to O(3) adversely affected small airway function.

Objectives: To investigate types of cancer caused by occupational exposure to vinyl chloride monomer (VCM) and the temporal mortality trends of these cancers in workers from polyvinyl chloride (PVC) manufacturing factories in Taiwan, with follow-up of the cohort extended by 15 years, from 1980 to 2007. Methods A retrospective cohort study of workers from six PVC factories in Taiwan was conducted. 3336 male PVC workers were enrolled and further linked with the National Mortality Registry and National Household Registry databases. Standardised mortality ratios (SMR) with 95% CIs were calculated and compared to the general Taiwanese male population. Cause-specific mortality between two study periods, 1980-1997 and 1998-2007, was compared. Six-year moving averages of the SMRs were calculated to examine mortality trends., Results: Liver cancer mortality increased during 1989-1994 (SMR 1.90, 95% CI 1.01 to 3.25), reached a peak during 1991-1996 (SMR 2.31, 95% CI 1.39 to 3.61) and became non-significant during 1994-1999 (SMR 1.42, 95% CI 0.80 to 2.34). Leukaemia mortality significantly increased during 1984-1989 (SMR 6.06, 95% CI 1.24 to 17.53), reached a peak during 1985-1990 (SMR 7.56, 95% CI 2.06 to 19.35) and became non-significant during 1991-1996 (SMR 3.24, 95% CI 0.39 to 11.69). The mortality trend for haemolymphopoietic cancer showed a similar pattern to that of leukaemia., Conclusions: VCM may increase the risk of liver cancer and leukaemia. When VCM exposure was controlled at worksites, mortality from these cancers returned to background levels.

Objectives: To investigate changes in blood pressure, blood lipids, blood sugar and haematological markers of inflammation associated with changes in long-term exposure to ambient air pollutants., Methods: We conducted secondary analyses of data on blood pressure and blood biochemistry markers from the Social Environment and Biomarkers of Aging Study in Taiwan and air pollution data from the Taiwan Environmental Protection Administration in 2000. Associations of 1-year averaged criteria air pollutants (particulate matter with aerodynamic diameters <10 μm (PM(10)) and <2.5 μm (PM(2.5)), ozone (O(3)), nitrogen dioxide (NO(2)), sulfur dioxide and carbon monoxide) with systolic blood pressure, diastolic blood pressure, total cholesterol, triglycerides, high-density lipoprotein cholesterol, fasting glucose, haemoglobin A1c (HbA1c), interleukin 6 (IL-6) and neutrophils were explored by applying generalised additive models., Results: After controlling for potential confounders, we observed that increased 1-year averaged particulate air pollutants (PM(10) and PM(2.5)) and NO(2) were associated with elevated blood pressure, total cholesterol, fasting glucose, HbA1c, IL-6 and neutrophils. Associations of increased 1-year averaged O(3) with elevated blood pressure, total cholesterol, fasting glucose, HbA1c and neutrophils were also observed. In particular, our two-pollutant models showed that PM(2.5) was more significantly associated with end-point variables than two gaseous pollutants, O(3) and NO(2)., Conclusions: Changes in blood pressure, blood lipids, blood sugar and haematological markers of inflammation are associated with long-term exposure to ambient air pollutants. This might provide a link between air pollution and atherosclerotic cardiovascular diseases.

Background: Most studies of the relationship between work and acute ischemic heart disease (IHD) were performed in western populations, and the extent to which their findings hold in Asian populations is largely unknown. The purpose of this study was to examine the association between job categories and non-fatal, first episodes of acute IHD in Taipei, Taiwan., Methods: A hospital-based, case-control design was used. Cases were patients with a first episode of non-fatal acute IHD who were admitted to the department of cardiology. Two controls without known cardiovascular disease were matched to each case for age, gender, and date of admission. A total of 119 cases and 238 controls were enrolled between April and September 2004., Results: Compared with white-collar workers, blue-collar workers had a 5.3-fold (95% CI: 1.5, 18.5) increased risk of a first episode of non-fatal acute IHD, while self-employed workers and managers/professionals had a slightly lower odds ratio of 0.6 (95% CI: 0.1, 2.4) and 0.5 (95% CI: 0.1, 2.2), respectively. Hypertension, diabetes, obesity, physical inactivity, and sleep disturbance were significant risk factors for acute IHD. A clustering of the cardiovascular risk factors was found in blue-collar workers., Conclusions: Blue-collar workers had a 5.3-fold increased risk of a first event of non-fatal acute IHD compared with white-collar workers, and this increased risk was associated with a clustering of cardiovascular risk factors.

In the present study, the cardiovascular toxicity of PM(2.5) was determined in spontaneously hypertensive (SH) rats using the standard deviation of normal-to-normal intervals (SDNN) and root mean square of successive differences of adjacent normal-to-normal intervals (RMSSD) as outcome measurements. Four SH rats implanted with radiotelemetry transmitters were repeatedly exposed to concentrated PM(2.5) in nose-only exposure chambers. Gravimetric analysis revealed the mean post-concentrating mass concentration of particles during the 5 h of exposure was 202 mug/m(3). Using each animal as its own control and linear mixed-effects model, to adjust for circadian nature and individual differences, we found that SDNN decreased by 15% initially then gradually decreased to 60% of the initial value at the end of exposure. Our results indicate that concentrated PM(2.5) may decrease SDNN on SH rats during PM exposure. The study also showed that SDNN is more sensitive to PM induced effects than RMSSD.

The association between vinyl chloride monomer (VCM) exposure and DNA damage has been established. However, the relationship between individual exposure and DNA single strand breaks was limited. Since environmental monitoring may not reflect the actual exposure, a useful marker of exposure is needed to assess the individual exposure. In our previous study, we have found a high correlation between air VCM level and urinary thiodiglycolic acid (TdGA) at the commencement of the next shift. Here, we further used comet assay to evaluate the relationship between urinary TdGA levels and DNA single strand breaks in polyvinyl chloride monomer (PVC) workers. Urinary TdGA levels (n=26) at the commencement of the following shift were analyzed. Ten of the 26 workers also had personal air sampling for air VCM exposure. Questionnaires were administered to obtain epidemiological information including detailed history of occupation and lifestyles. Workers experiencing air VCM level greater than 5 ppm had higher tail moment and tail intensity (%) than those experiencing VCM exposure between 1 and 5, or <1 ppm, respectively (P < 0.05). The results also revealed that level of DNA single strand breaks, including tail moment and tail intensity, were increased with urinary TdGA level. The dose-response relationship of urinary TdGA level and DNA single strand breaks was particularly significant among the workers with 4 mg/g Cr of urinary TdGA level, which is equivalent to 5 ppm air VCM level. We concluded that air VCM exposure greater than 5 ppm could induce DNA damage. Further sensitive assay should be developed for the diction of DNA damage when air VCM exposure below 5 ppm.

The health impact of dust events from China has become a concern within China and in its neighboring countries. Previous epidemiological studies have demonstrated an association between particulate matter exposure and cardiopulmonary mortality. Here, we use pulmonary hypertensive rat models to examine inflammation markers in the lung and in peripheral blood after exposure to Asian dust storm particles. Using a nose-only inhalation system, eight pulmonary hypertensive rats were exposed to concentrated ambient particles (CAPs) from an actual Asian dust storm that took place between March 18 and 19, 2002; four control rats were also exposed to room air. Four rats exposed to CAPs of 315.6 g/m3 for 6 h were classified as the low-exposure group, and another four rats exposed to CAPs of 684.5 g/m3 for 4.5 h were classified as the high-exposure group. The animals were sacrificed 36 h after exposure. Inflammation markers in the peripheral blood and in the bronchoalveolar lavage (BAL) were analyzed, and IL-6 in BAL was also determined using ELISA. White blood cell counts in peripheral blood increased with increased CAP exposure levels (P<0.001, test for trend). In BAL analysis, total cell numbers and the proportion of neutrophil also increased with increased CAP levels (P<0.001, test for trend for both markers). Positive dose-response relationships between CAP exposure and total protein (P<0.05) and between CAPs and LDH activity (P<0.05) were also observed. Moreover, IL-6 protein in BAL increasing with CAP levels (P<0.05, test for trend) was demonstrated. Our results revealed that exposure to particulate matters during an Asian dust storm could increase lung inflammation and injury in pulmonary hypertensive rats. Further studies are needed to determine the components of dust storm particles that may contribute to the particle toxicity.

Epichlorohydrin (1-chloro-2,3,-epoxypropane; ECH) is a strong irritant of the eyes, respiratory tract, and skin. Because the toxic effect of various chemicals can be modified by metabolic traits, in this study, we also investigated the influence of the glutathione S-transferase (GSTM1) and (GSTT1) genes on the toxic effect of ECH. In the GSTM1 null genotype workers, there is a dose-response of lung function tests (FEV1, FEV1/FVC, MMEF) for ECH exposure, but not in the GSTM1 non-null genotype workers. The ECH exposure was found to be significantly associated with a decreased FEV1 value (P = 0.09) and a decreased MMEF value (P = 0.053) after adjusting for other factors. The GSTM1 null genotype was found to be significantly associated with a decreased FEV1 value (P = 0.038), decreased FEV1/FVC value (P = 0.056), and decreased MMEF value (P = 0.012) after adjusting for other factors. This study indicates that obstructive lung abnormalities and small airway lung damage are associated with ECH exposure, and ECH workers with GSTM1 null-type are also associated with increased respiratory damage.

Background: Epichlorohydrin (ECH) is a strong irritant of the eyes, respiratory tract, and skin. The aims of this study were to examine the dose-response relationship between observed abnormal pulmonary function tests and respiratory tract irritation symptoms among epichlorohydrin-exposed workers in Taiwan., Methods: A total of 167 workers were randomly selected from a resin synthesis factory. Sixty-six air samples were taken to determine ECH concentration in the workplace. Demographic data, work history, smoking status, and respiratory tract irritation symptoms were gathered by a standard self-administered questionnaire. Pulmonary function tests were also performed., Results: There were 13 of 41 (31.7%) abnormal mean mid-expiratory flow (MMEF) among the high-ECH-exposed workers, 11 of 38 (29%) among the low-ECH-exposed workers, and 4 of 59 (6.8%) among non-ECH-exposed workers. There was a significant linear trend between ECH exposure and the prevalence of small airway abnormalities (P = 0.007) after adjusting for other factors. There was also a significant dose-response relationship of respiratory tract irritation symptoms (cough, phlegm, chest tightness, and dyspnea) among the ECH-exposed workers., Conclusions: This study suggests that obstructive lung abnormalities and small airway lung damage are associated with ECH exposure. The study also suggests that exposure to very low concentrations (<0.2 ppm) causes significant higher prevalence of respiratory tract irritation symptoms. Causal inferences from the findings cannot be made from this cross-sectional study and further longitudinal studies are needed to better clarify the nature of the observed associations., (Copyright 2003 Wiley-Liss, Inc.)

Challenges facing a developing country during transition to newly developed status include lack of: a hazard communication system, a prudent industrial zoning policy, and occupational safety and health (OSH) technology and personnel. The authors offer an approach to the future that encompasses implementation of a pollution prevention system, comprehensive coverage of occupational injuries and diseases, and integration of information technology with OSH protection.

Mutant p53 protein and anti-p53 antibody in circulating blood can be detectedamong individuals with mutations of the p53 tumor suppressor gene. Plasma mutant p53 protein and anti-p53 antibody have also been associated with vinyl chloride monomer (VCM) exposure, although the mechanism of VCM-related carcinogenesis remains unclear. Polymorphisms of metabolic and DNA repair genes have been implicated in chemical exposure-related carcinogenesis. The aim of this study is to explore the association between polymorphisms of metabolic and DNA repair genes with mutant p53 protein and anti-p53 antibody expression induced by VCM. Study subjects comprised 333 male workers occupationally exposed to VCM. Plasma mutant p53 protein and anti-p53 antibody detected with ELISA were grouped together as p53 overexpression. Genotypes of cytochrome P450 2E1 (CYP2E1), aldehyde dehydrogenase 2 (ALDH2), glutathione S-transferase T1 (GSTT1), and X-ray repair cross-complementing group 1 (XRCC1, exon 10) genes were identified by the PCR. High VCM exposure group had significantly higher p53 overexpression as compared with low exposure group [odds ratio (OR), 2.1; 95% confidence interval (CI), 1.1-3.8]. Individuals having experienced a high VCM exposure and displaying a XRCC1 Gln-Gln genotype had a highest risk of p53 overexpression among those having different combinations of VCM exposure and XRCC1 genotypes (OR, 6.5; 95% CI, 1.7-24.2). Interestingly, those subjects reflecting a CYP2E1 c2c2 genotype among the low VCM-exposure group demonstrated a greater risk of p53 overexpression (OR, 9.8; 95% CI, 1.2-81.6) as compared with those experiencing a low VCM exposure and CYP2E1 c1c1/c1c2 genotypes. Additional analysis revealed that individuals possessing more susceptible XRCC1 Gln-Gln, CYP2E1 c2c2, ALDH2 1-2/2-2, and non-null GSTT1 genotypes were more likely to reveal p53 overexpression. Our results suggest that susceptible XRCC1 and CYP2E1 genotypes may modulate the mutation of the p53 gene among VCM-exposed workers.