The roles of lumbar load thresholds in cumulative lifting exposure to predict disk protrusion in an Asian population.

BACKGROUND: The purpose of this study was to determine whether a specific threshold per lifting movement, the accumulation above which best predicts lumbar disk protrusion, exists or the total lifting load should be considered. METHODS: This was a retrospective study. Subjects with various lifting exposures were recruited. Disk protrusion was assessed by magnetic resonance imaging. The cumulative lifting load was defined as the sum of the time-weighed lumbar load for each job and was calculated using a biomechanical software system. The effectiveness of accumulation above different thresholds in predicting disk protrusion were compared using four statistical methods. RESULTS: A total of 252 men and 301 women were included in the final analysis. For the men, 3000 Newtons for each lifting task was the optimal threshold for predicting L4-S1 disk protrusion, whereas for the women, 2800 Newtons was optimal. CONCLUSIONS: Our findings suggested that for cumulative lifting exposure, including the total lifting load without defining a minimal exposure limit might not be the optimal method for predicting disk protrusion. The NIOSH 3400 Newton recommended limits do not appear to be the optimal thresholds for preventing disk protrusion. Different lifting thresholds might be needed for men and women in the workplace for their safety.

Professional Driver's Job Stress and 8-year Risk of Cardiovascular Disease: The Taiwan Bus Driver Cohort Study.

BACKGROUND: Two main job stress models-the Demand-Control-Support (DC) model and the Effort-Reward Imbalance (ERI) model have been used to assess the impact of psychosocial work-related factors for cardiovascular disease (CVD). Limited evidence elaborates the independent and combined effects on CVD events, especially for professional drivers. This study assesses the independent and combined effects of DC and ERI models on an 8-year risk of CVD among professional drivers. METHODS: The Taiwan Bus Driver Cohort Study recruited 1650 professional drivers from a large bus company in 2005. The subjects were interviewed in person and completed the two job stress questionnaires. Researchers found 94 new cases of CVD (International Classification of Diseases, Ninth Revision, Clinical Modification [ICD-9-CM]: 390-459) from 2006 to 2012. A Cox proportional hazards model was performed to estimate the hazard ratio (HR) for CVD events. RESULTS: Occupational drivers with high overcommitment scores (thresholds of 15) had an elevated risk for CVD (HR = 1.71; 95% CI = 1.04, 2.82). Regarding target disease, overcommitment had an increased risk for CVD (not including hypertensive disease) (HR = 1.27; 95% CI = 1.05, 1.54) and ischemic heart disease (HR = 1.32; 95% CI = 1.05-1.65). CONCLUSION: Overcommitment, which is associated with job stress, appears to be associated with CVD risk in professional drivers.

Effects of nanoparticles exposure and PON1 genotype on heart rate variability.

OBJECTIVES: This study was to assess the association between different NPs exposure and PON1 genotype on Heart Rate Variability (HRV) parameters among workers. METHODS: This study included 235 non-CVD subjects handled to nanomaterials (NM) and 185 non-exposed controls without CVD from 14 NM plants. All participants completed short-term HRV measurements, and were collected blood specimens to measure PON1 activities and the genotype of the PON1 Q192R polymorphism. RESULTS: In a multivariate regression model, this study observed a positive relationship between nano-Ag exposure and HRV time-domain (RMSSD) and frequency-domain (HF). After adjusting for confounders, the results showed positive associations between RR homozygosity, PON1 paraoxonase/arylesterase activities with HRV, and was particularly noteworthy in RMSSD and HF. CONCLUSIONS: This study shows a significant increment of RMSSD and HF among workers who handled Nano-Ag materials. These results imply that Nano-Ag and PON1 Q192R genotype can trigger ANS reflexes and alter cardiac frequency and function.

Longitudinal follow-up of health effects among workers handling engineered nanomaterials: a panel study.

BACKGROUND: Although no human illness to date is confirmed to be attributed to engineered nanoparticles, occupational epidemiological studies are needed to verify the health effects of nanoparticles. This study used a repeated measures design to explore the potential adverse health effects of workers handling nanomaterials. METHODS: Study population was 206 nanomaterial-handling workers and 108 unexposed controls, who were recruited from 14 nanotechnology plants. They were followed up no less than two times in four years. A questionnaire was used to collect potential confounders and detailed work conditions. Control banding was adopted to categorize risk level for each participant as a surrogate marker of exposure. Health hazard markers include cardiopulmonary dysfunction markers, inflammation and oxidative damage markers, antioxidant enzymes activity, and genotoxicity markers. The Generalized Estimating Equation model was applied to analyze repeated measurements. RESULTS: In comparison to the controls, a significant dose-dependent increase on risk levels for the change of superoxide dismutase (p<0.01) and a significant increase of glutathione peroxidase change in risk level 1 was found for nanomaterial-handling workers. However, the change of cardiovascular dysfunction, lung damages, inflammation, oxidative damages, neurobehavioral and genotoxic markers were not found to be significantly associated with nanomaterials handling in this panel study. CONCLUSIONS: This repeated measurement study suggests that there was no evidence of potential adverse health effects under the existing workplace exposure levels among nanomaterials handling workers, except for the increase of antioxidant enzymes.

Measurement of urinary arsenic profiles and DNA hypomethylation in a case-control study of urothelial carcinoma.

Environmental exposure to arsenic may be involved in the disturbance of DNA hypomethylation. The aim of this study is the first to explore the effect of interactions of urinary total arsenic levels, arsenic methylation capacity, 8-hydroxy-2'-deoxyguanosine (8-OHdG), plasma folate, and global 5-methyl-2'-deoxycytidine (5-MedC) levels on the risk of urothelial carcinoma (UC). A hospital-based case-control study was constructed. The research involved the histological recruitment and pathological verification of 178 UC patients and 356 age-/sex-matched controls without prior history of cancer. Arsenic species were determined by high-performance liquid chromatography (HPLC)-hydride generation and atomic absorption. 5-MedC levels were detected by HPLC and triple-quadrupole mass spectrometry (MS). 8-OHdG was processed by an online solid-phase extraction LC-MS/MS. Plasma folate levels were measured using the chemiluminescent technology. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by multiple logistic regression analysis. Results indicate that the high levels of total urinary arsenic, inorganic arsenic percentage, and 8-OHdG and the low levels of DMA % and plasma folate were independent factors of UC. In addition, global 5-MedC levels in the first quartile versus fifth quartile significantly increased the twofold OR of UC after potential factors were adjusted (95% CI:1.10-4.03). The interaction of 5-MedC level and high total arsenic level, insufficient arsenic capacity, high 8-OHdG, and low folate levels was insignificant. Results of stepwise logistic regression analysis indicate that high total urinary arsenic levels (Q3 versus Q1), low plasma folate level, and low global 5-MedC (Q4 versus Q5) significantly increased the ORs of UC. The above results suggest that high total arsenic, low plasma folate, and 5-MedC levels affect the ORs of UC independently.

Risk of Alzheimer's disease with metal concentrations in whole blood and urine: A case-control study using propensity score matching.

Environmental exposure to heavy metals is suspected to result in neuropathology damage and cognitive impairment. We aimed to explore the association of Alzheimer's disease (AD) risk with the internal dose of heavy metals by constructing a hospital-based case-control study and using propensity-score-matching methods. We investigated 170 patients with AD and 264 controls from the Department of Neurology and Family Medicine, China Medical University Hospital in Taiwan. All patients with AD received clinical neuropsychological examination and cognitive-function assessments, including the mini-mental status examination and clinical dementia rating scale. We also constructed a propensity-score-matched population of 82 patients with AD and 82 controls by matching age, gender, education, and AD-related comorbidity. Blood levels with cadmium, lead, mercury, selenium, and urinary arsenic profile were measured. Logistic regression models and 95% confidence intervals (CIs) were applied to estimate AD risk. After stratification by respective quartile cutoffs of heavy metals, the AD risk of study participants with high urinary inorganic arsenic (InAs%) or low dimethylarsinic acid (DMA%) significantly increased (p < 0.05), as similarly found in the propensity-score-matched population. In addition, people with a low median level of selenium and high median level of InAs%, or/and a low median level of DMA% had approximately two- to threefold significant AD risk. Urinary arsenic profiles may be associated with increased AD risk. Repeat measurements of heavy metals with large sample size and the surveying of potential exposure sources are recommended in future studies.

Relationships among DNA hypomethylation, Cd, and Pb exposure and risk of cigarette smoking-related urothelial carcinoma.

Cigarette smoking and environmental exposure to heavy metals are important global health issues, especially for urothelial carcinoma (UC). However, the effects of cadmium and lead exposure, as well as the levels of DNA hypomethylation, on UC risk are limited. We evaluated the possible exposure sources of Cd and Pb and the relationship among DNA hypomethylation, urinary Cd and Pb levels, and UC risk. We recruited 209 patients with UC and 417 control patients for a hospital-based case-control study between June 2011 and August 2014. We collected environmental exposure-related information with questionnaires. Blood and urine samples were analyzed to measure the Cd and Pb exposure and 5-methyl-2'-deoxycytidine levels as a proxy for DNA methylation. Multivariate logistic regression and 95% confidence intervals were applied to estimate the risk for UC. Study participants with high Cd and Pb exposure in blood or urine had significantly increased risk of UC, especially among the smokers. After adjusting for age and gender, the possible connections of individual cumulative cigarette smoking or herb medicine exposure with the increased levels of Cd and Pb were observed in the controls. Participants with 8.66%-12.39% of DNA hypomethylation had significantly increased risk of UC compared with those with ≥12.39% of DNA hypomethylation. Environmental factors including cigarette smoking and herb medicine may contribute to the internal dose of heavy metals levels. Repeat measurements of heavy metals with different study design, detailed dietary information, and types of herb medicine should be recommended for exploring UC carcinogenesis in future studies.

Effect of CYP3A4 genetic polymorphisms on the genotoxicity of 4,4'-methylene-bis(2-chloroaniline)-exposed workers.

OBJECTIVES: We investigated the relationship between 4,4'-methylene-bis(2-chloroaniline) (MBOCA) exposure and micronucleus (MN) frequency, and how this association was affected by genetic polymorphism of the cytochrome P450 enzyme (CYP3A4). METHODS: We divided the study population into an exposed group (n=44 with total urine MBOCA ≥20 µg/g creatinine) and a control group (n=47 with total urine MBOCA <20 µg/g creatinine). Lymphocyte MN frequency (MNF) and micronucleated cell (MNC) frequency were measured by the cytokinesis-block MN assay method. MNF reported as the number of micronuclei in binucleated cells per 1000 cells, and MNC reported as the number of binucleated cells with the presence of MN per 1000 cells. CYP3A4 alleles were measured by PCR-based restriction fragment length polymorphism (PCR-RFLP). RESULTS: The mean MNF (6.11 vs 4.46 MN/1000 cells, p<0.001) and MNC (5.75 vs 4.15 MN/1000 cells, p<0.001) in the exposed workers was significantly higher than that in the controls. The CYP3A4 polymorphism A/A+A/G influenced the difference in the mean MNF (5.97 vs 4.38 MN/1000 cells, p<0.001) and MNC (5.60 vs 4.15 MN/1000 cells, p<0.001) between the MBOCA-exposed and control groups. After adjusting risk factors, the MNF level in the MBOCA-exposed workers was 0.520 MN cells/1000 cells (p<0.001) higher than the control group among the CYP3A4 A/A+A/G genotype. Similarly, the MNC level in the MBOCA-exposed workers was 0.593 MN/1000 cells (p<0.001) higher than the control group among the CYP3A4 A/A+A/G genotype. However, the difference in adjusted MNF and MNC between the exposed and control groups was not significant for the CYP3A4 polymorphism with the G/G genotype. CONCLUSIONS: We recommend that lymphocytes MNF and MNC are good indicators to evaluate MBOCA genotoxicity. Individuals with the CYP3A4 polymorphism A/A and A/G genotypes appear to be more susceptible to MBOCA genotoxicity.

Increased levels of oxidative stress biomarkers in metal oxides nanomaterial-handling workers.

This study assessed oxidatively damaged DNA and antioxidant enzyme activity in workers occupational exposure to metal oxides nanomaterials. Exposure to TiO2, SiO2, and ITO resulted in significant lower antioxidant enzymes (glutathione peroxidase and superoxide dismutase) and higher oxidative biomarkers 8-hydroxydeoxyguanosine (8-oxodG) than comparison workers. Statistically significant correlations were noted between plasma and urine 8-oxodG, between white blood cells (WBC) and urine 8-oxodG, and between WBC and plasma 8-oxodG. In addition, there were significant negative correlations between WBC 8-oxodG and SOD and between urinary 8-oxodG and GPx levels. The results showed that urinary 8-oxodG may be considered to be better biomarker.

Association between levels of urinary heavy metals and increased risk of urothelial carcinoma.

OBJECTIVES: To evaluate possible sources of exposure to heavy metals in the general population, and to determine the association between urinary heavy metals and urothelial carcinoma risk. METHODS: We recruited 205 patients with urothelial carcinoma and 406 control participants for a case-control study between June 2011 and December 2013. The control participants were frequency-matched with cases according to sex and age. We measured the urinary levels of arsenic, cadmium, chromium, nickel and lead by using inductively coupled plasma mass spectrometry. We collected environmental exposure-related information through questionnaires. Multivariate logistic regression and 95% confidence intervals were applied to estimate the urothelial carcinoma risk and potential effects of urothelial carcinoma-related risk factors on the levels of urinary heavy metals. RESULTS: Patients with urothelial carcinoma showed higher urinary levels of arsenic, cadmium, chromium, nickel and lead than the controls. After considering other potential risk factors, a significantly increased risk for urothelial carcinoma was observed in patients with increased urinary levels of cadmium, chromium, nickel and lead. Smokers showed a high urinary cadmium level. In addition to cadmium, a high urinary lead level was associated with cumulative cigarette smoking and herbal medicine use. CONCLUSION: Environmental factors might contribute to higher urinary levels of heavy metals and ultimately result in urothelial carcinoma carcinogenesis. These findings can promote proper environmental surveillance of exposure to heavy metals in the general population.

Potential Association of Urinary N7-(2-Carbamoyl-2-hydroxyethyl) Guanine with Dietary Acrylamide Intake of Smokers and Nonsmokers.

Acrylamide (AA), a rodent carcinogen, is widely used in industry and present in cigarette smoke as well as in foods processed at high temperatures. The metabolic activation of AA to glycidamide (GA) could be critical for AA carcinogenicity since GA causes DNA adduct formation in vivo. N7-(2-carbamoyl-2-hydroxyethyl) guanine (N7-GAG), the most abundant DNA adduct of AA, is subjected to spontaneous and enzymatic depurination and excreted through urine. Urinary N7-GAG analysis can confirm AA genotoxicity and identify active species of AA metabolites in humans, thereby serving as a risk-associated biomarker for molecular epidemiology studies. This study aimed to develop an isotope-dilution solid-phase extraction liquid chromatography tandem mass spectrometry method to comparatively analyze urinary N7-GAG levels in nonsmokers and smokers. Urinary N-acetyl-S-(propionamide)-cysteine (AAMA), a metabolite of AA, was also analyzed as a biomarker for current AA exposure. Urinary N7-GAG was quantified by monitoring m/z 239 → 152 for N7-GAG and m/z 242 → 152 for (13)C3-labeled N7-GAG under positive electron spray ionization and multiple reaction mode. The median urinary N7-GAG level was 0.93 µg/g creatinine in nonsmokers (n = 33) and 1.41 µg/g creatinine in smokers (n = 30). Multiple linear regression analysis of data revealed that N7-GAG levels were only significantly associated with AAMA levels. These results demonstrate that urinary N7-GAG of nonsmokers and smokers is significantly associated with a very low level of dietary AA intake, assessed by analyzing urinary AAMA.

The impact of obstructive sleep apnea on high-sensitivity C-reactive protein in subjects with or without metabolic syndrome.

BACKGROUND: It is unclear whether obstructive sleep apnea (OSA) is independently associated with increased levels of the acute-phase reactant C-reactive protein (CRP). The purpose of this study was to evaluate the relationship between OSA and high-sensitivity CRP (hs-CRP) levels according to the presence or absence of metabolic syndrome (MetS). METHODS: This study recruited 245 male bus drivers from one transportation company in Taiwan. Each participant was evaluated by a polysomnography (PSG) test, blood lipids examination, and hs-CRP. Severity of OSA was categorized according to the apnea-hypopnea index (AHI). RESULTS: Subjects were categorized into severe OSA group (n = 44; 17.9 %), moderate and mild OSA group (n = 117; 47.8 %), and non-OSA group (n = 84; 34.3 %). AHI had a significant association with hs-CRP (ß = 0.125, p = 0.009) adjusting for age, smoking, drinking, and MetS status. Hs-CRP was elevated with severe OSA (ß = 0.533, p = 0.005) even adjusting for BMI and MetS. Moreover, there was an independent effect for adjusted odds ratios (AORs) between the stratification of the severity for OSA and MetS. CONCLUSION: Elevated hs-CRP level is associated with severe OSA, independent of known confounders. The effect of OSA in CRP is independent of MetS was identified.

Cancer incidence of Taiwanese shipbreaking workers who have been potentially exposed to asbestos.

BACKGROUND: Shipbreaking remains one of the most dangerous jobs worldwide. Shipbreaking workers are exposed to many hazardous chemicals, especially asbestos. Unfortunately, long-term follow-up studies of cancer incidence patterns in shipbreaking workers are lacking. This study examines whether there is an increased risk of cancer among male shipbreaking workers over a 24-year follow-up period. METHODS: 4155 male shipbreaking worker's information was retrospectively collected from Kaohsiung's Shipbreaking Workers Union database from 1985. The study cohort was linked to the Taiwan Cancer Registry from 1985 to 2008 for new cancer cases. The expected number of cancers for shipbreaking workers was calculated by using the age (5-year intervals) and calendar time-specific annual rates of cancer incidence with reference to the general population of Taiwan from 1985 to 2008. Standardized incidence ratios (SIRs) were calculated as relative risk estimates. The hazard ratio (HR) for cancer was calculated for the shipbreaking workers with Total Exposure Potential Scores for asbestos. RESULTS: After consideration of a 5-year latency period, an elevated incidence of overall cancer (N=368; SIR=1.13 (1.01-1.25)), oral cavity cancer (N=83; SIR=1.99 (1.58-2.46)), and trachea, bronchus, and lung cancers (N=53; SIR=1.36 (1.02-1.78)) was found among male shipbreaking employees. Moreover, mesothelioma cases were found in those who had the occupation of flame cutter. The high asbestos exposure group was associated with an increased SIR of developing overall cancer and oral cancer, whether we considered a 5-year or 10-year latency period. CONCLUSION: Asbestos-related diseases, including lung cancer and mesothelioma, were seen in excess in these shipbreaking workers and some cases appeared to have a dose-dependent relationship. Preventative measures among male shipbreaking workers should be researched further.

Short-term effects of fine particulate air pollution on hospital admissions for respiratory diseases: a case-crossover study in a tropical city.

This study was undertaken to determine whether there was a correlation between fine particles (PM2.5) levels and hospital admissions for respiratory diseases in Kaohsiung, Taiwan. Hospital admissions for respiratory diseases including pneumonia, asthma, and chronic obstructive pulmonary disease (COPD) and ambient air pollution data for Kaohsiung were obtained for the period 2006-2010. The relative risk (RR) of hospital admissions for respiratory diseases was estimated using a case-crossover approach, controlling for weather variables, day of the week, seasonality, and chronic time trends. For the single-pollutant model (without adjustment for other pollutants), increased number of admissions for respiratory diseases were significantly associated with higher PM2.5 levels only on cool days (<25°C), with an interquartile range rise associated with a 50 (95% CI% = 45-55%), 40% (95% CI = 25-58%), and 46% (95% CI = 36-57%) elevation in frequency of admissions for pneumonia, asthma, and COPD, respectively. In the two-pollutant models, PM2.5 levels remained significant even controlling for sulfur dioxide, nitrogen dioxide, carbon monoxide, or ozone on cool days. This study provides evidence that higher levels of PM2.5 increase the risk of hospital admissions for respiratory diseases in Taiwan.

Effect of nanoparticles exposure on fractional exhaled nitric oxide (FENO) in workers exposed to nanomaterials.

Fractional exhaled nitric oxide (FENO) measurement is a useful diagnostic test of airway inflammation. However, there have been few studies of FENO in workers exposed to nanomaterials. The purpose of this study was to examine the effect of nanoparticle (NP) exposure on FENO and to assess whether the FENO is increased in workers exposed to nanomaterials (NM). In this study, both exposed workers and non-exposed controls were recruited from NM handling plants in Taiwan. A total of 437 subjects (exposed group = 241, non-exposed group = 196) completed the FENO and spirometric measurements from 2009-2011. The authors used a control-banding (CB) matrix to categorize the risk level of each participant. In a multivariate linear regression analysis, this study found a significant association between risk level 2 of NP exposure and FENO. Furthermore, asthma, allergic rhinitis, peak expiratory flow rate (PEFR), and NF-κB were also significantly associated with FENO. When the multivariate logistic regression model was adjusted for confounders, nano-TiO2 in all of the NM exposed categories had a significantly increased risk in FENO > 35 ppb. This study found associations between the risk level of NP exposure and FENO (particularly noteworthy for Nano-TiO2). Monitoring FENO in the lung could open up a window into the role nitric oxide (NO) may play in pathogenesis.

Longitudinal assessment of oxidative stress markers and their relationship with exposure to PM2.5 and its bound metals in healthy participants.

OBJECTIVE: Exposure to ambient PM2.5 and its bound metals poses a risk to health and disease, via, in part, oxidative stress response. A variety of oxidative stress markers have been used as markers of response, but their relevance to environmental exposure remains to be established. We evaluated, longitudinally, a battery of oxidative stress markers and their relationship with the exposure of PM2.5 and its bound metals in a panel of healthy participants. MATERIAL AND METHODS: Levels of residence- and personal-based ambient air PM2.5 and its bound metals, as well as of lung function parameters, were assessed in a total of 58 questionnaire-administered healthy never smoker participants (male, 39.7%). Levels of urinary oxidative stress markers, including Nε-(hexanoyl)-lysine (HEL; an early lipid peroxidation product), 4-hydroxynonenal (4-HNE), N7-methylguanine (N7-meG), and 8-hydroxy-2-deoxyguanosine (8-OHdG), plasma antioxidants [superoxide dismutase (SOD) and glutathione peroxidase (GPx), and urinary metals were measured by ELISA, LC-MS, and ICP-MS, respectively. The results of three repeated measurements at two-month intervals were analyzed using the Generalized Estimating Equation (GEE). RESULTS: After adjusting for confounders, residence- and personal-based PM2.5 levels were positively associated with HEL (ß = 0.22 and 0.18) and N7-meG (ß = 0.39 and 0.13). Significant correlations were observed between personal air PM2.5-Pb and urinary Pb with HEL (ß = 0.08 and 0.26). While FVC, FEV1, FEV1/FVC, MMF, and PEFR predicted% were normal, a negative interaction (pollutant*time, P < 0.05) was noted for PM2.5-V, Mn, Co, Ni, Zn, As, and Pb. Additionally, a negative interaction was found for N7-meG (ß = -21.35, -18.77, -23.86) and SOD (ß = -26.56, -26.18, -16.48) with FEV1, FVC, and PEFR predicted%, respectively. CONCLUSION: These findings emphasize potential links between environmental exposure, internal dose, and health effects, thereby offering valuable markers for future research on metal exposure, oxidative stress, and health outcomes.

Crucial role of Toll-like receptors in the zinc/nickel-induced inflammatory response in vascular endothelial cells.

Our previous studies indicated that zinc induced inflammatory response in both vascular endothelial cells and promonocytes. Here, we asked if other metals could cause the similar effect on vascular endothelial cells and tried to determine its underlying mechanism. Following screening of fifteen metals, zinc and nickel were identified with a marked proinflammatory effect, as determined by ICAM-1 and IL-8 induction, on human umbilical vein endothelial cells (HUVECs). Inhibiting protein expression of myeloid differentiation primary response protein-88 (MyD88), a Toll-like receptor (TLR) adaptor acting as a TLR-signaling transducer, significantly attenuated the zinc/nickel-induced inflammatory response, suggesting the critical roles of TLRs in the inflammatory response. Blockage of TLR-4 signaling by CLI-095, a TLR-4 inhibitor, completely inhibited the nickel-induced ICAM-1 and IL-8 expression and NFκB activation. The same CLI-095 treatment significantly blocked the zinc-induced IL-8 expression, however with no significant effect on the ICAM-1 expression and a minor inhibitory effect on the NFκB activation. The finding demonstrated the differential role of TLR-4 in regulation of the zinc/nickel-induced inflammatory response, where TLR-4 played a dominant role in NFκB activation by nickel, but not by zinc. Moreover, inhibition of NFκB by adenovirus-mediated IκBα expression and Bay 11-7025, an inhibitor of cytokine-induced IκB-α phosphorylation, significantly attenuated the zinc/nickel-induced inflammatory responses, indicating the critical of NFκB in the process. The study demonstrates the crucial role of TLRs in the zinc/nickel-induced inflammatory response in vascular endothelial cells and herein deciphers a potential important difference in NFκB activation via TLRs. The study provides a molecular basis for linkage between zinc/nickel exposure and pathogenesis of the metal-related inflammatory vascular disease.

Fine particulate air pollution and hospital admissions for myocardial infarction in a subtropical city: Taipei, Taiwan.

This study was undertaken to determine whether there was a correlation between fine particles (PM2.5) levels and hospital admissions for myocardial infarction (MI) in Taipei, Taiwan. Hospital admissions for MI and ambient air pollution data for Taipei were obtained for the period 2006-2010. The relative risk of hospital admissions for MI was estimated using a casecrossover approach, controlling for weather variables, day of the week, seasonality, and longterm time trends. For the single-pollutant model (without adjustment for other pollutants), increased numbers of MI admissions were significantly associated with higher PM2.5 levels both on warm days (>23°C) and on cool days (<23°C). This was accompanied by an interquartile range elevation correlated with a 10% (95% CI = 6-15%) and 5% (95% CI = 1-9%) rise in number of MI admissions, respectively. In the two-pollutant models, PM2.5 remained significant after inclusion of SO2 or O3 on both warm and cool days. This study provides evidence that higher levels of PM2.5 increase the risk of hospital admissions for MI.

Mortality among shipbreaking workers in Taiwan--a retrospective cohort study from 1985 to 2008.

BACKGROUND: Shipbreaking workers are typically exposed to a wide range of hazardous chemicals. However, long-term follow-up studies of their mortality patterns are lacking. This study examined mortality among shipbreaking workers over a 24-year follow-up period. METHODS: A total of 4,962 shipbreaking workers were recruited from the database of the Kaohsiung Shipbreaking Workers Union. The data were then linked to the Taiwan National Death Registry from 1985 to 2008. The mortality ratios-standardized for age and calendar years-(SMRs) for various causes of deaths were calculated with reference to the general population of Taiwan. RESULTS: Among men workers, a statistically significant increased SMR was observed for all causes (SMR = 1.28), all cancers (SMR = 1.26; particularly noteworthy for lesions of oral and nasopharyngeal: SMR 2.03, liver: SMR 4.63, and lung: SMR 1.36), cirrhosis of the liver (SMR = 1.32), and accidents (SMR = 1.91). A statistically significant increase in mortality was observed for respiratory system cancer (SMR = 1.87) and lung cancer (SMR = 1.91) among workers with a longer duration of employment (≥7 years). The result also showed that among shipbreaking workers who were still alive, two people had mesothelioma and 10 people have asbestosis. CONCLUSIONS: Those employed in shipbreaking industries experienced an increase in mortality from all causes. The increased SMR for lung cancer was probably related to asbestos, metals, and welding fume exposure.

Estimation of benefit of prevention of occupational cancer for comparative risk assessment: methods and examples.

OBJECTIVES: To quantify the life years gained and financial savings by preventing a case of occupational cancer. METHODS: The authors retrieved data from the Taiwan Cancer Registry and linked them with the National Mortality Registry to estimate the survival functions for major occupational cancers: lung, pleural mesothelioma, urinary bladder and leukaemia. Assuming a constant excess hazard for each type of cancer, the authors extrapolated lifetime survival functions by the Monte Carlo method. For each patient with cancer, the authors simulated an age- and gender-matched person without cancer based on vital statistics of Taiwan to estimate life expectancy and expected years of life lost (EYLL). By using the reimbursement data from the National Health Insurance Research Database, the authors calculated the average monthly healthcare expenditures, which were summed to estimate the lifetime healthcare expenditures after adjusting for the corresponding monthly survival probability. RESULTS: A total of 51,408, 136, 12,891 and 5285 new cases of lung, pleural mesothelioma, bladder and leukaemia cancers, respectively, were identified during 1997-2005 and followed until the end of 2007. The EYLL was predicted to be 13.7±0.1, 18.9±0.7, 4.7±0.3 and 19.4±0.5 years for these cancers, respectively, and the lifetime healthcare expenditures with a 3% annual discount were predicted to be US$22,359, US$14,900, US$51,987 and US$59,741, respectively. CONCLUSIONS: The burden of these occupational cancers, in terms of EYLL and lifetime healthcare expenditures, was substantial. Such estimates may provide useful empirical evidence for comparative risk assessment that can be applied in health policy-making and clinical decision-making.