The relationship between heated cigarette smoking and blood white blood cell count: a population-based cross-sectional study.

OBJECTIVES: Conventional cigarette smoking increases inflammation and white blood cell (WBC) counts. However, there have been limited studies on the relationship between heated cigarette smoking and WBC counts. This study aimed to examine this relationship using nationally representative population-based health data. STUDY DESIGN: This was a population-based cross-sectional study. METHODS: The Korea National Health and Nutrition Examination Survey database was used to analyze this relationship. Data related to sex, age, body mass index (BMI), WBC count, and smoking history were obtained from the database. The smoking-related questionnaires included smoking status, smoking type (heated or conventional cigarettes), and smoking amount. The summary statistics of the WBC counts were calculated according to sex, smoking status, and smoking type. In addition, the exposure-response relationship between the smoking amount and WBC count was examined by smoking type, controlling for sex, age, and BMI. RESULTS: In total, 9747 WBC measurements were used in the analyses. WBC count increased in conventional cigarette smokers, while there was no significant difference in WBC count between heated cigarette smokers and non-smokers. The WBC count showed a positive dose-response relationship with the smoking amount in both conventional and heated cigarette smokers. CONCLUSIONS: The results confirm that conventional cigarette smoking increases WBC counts. Furthermore, the results suggest that heated cigarette smoking does not lead to a significant increase in WBC counts, although it indicates a potential dose-response relationship with WBC count. Further research with larger sample sizes is needed to confirm whether these results reflect true associations.

Estimating retrospective exposure of household humidifier disinfectants.

UNLABELLED: We conducted a comprehensive humidifier disinfectant exposure characterization for 374 subjects with lung disease who presumed their disease was related to humidifier disinfectant use (patient group) and for 303 of their family members (family group) for an ongoing epidemiological study. We visited the homes of the registered patients to investigate disinfectant use characteristics. Probability of exposure to disinfectants was determined from the questionnaire and supporting evidence from photographs demonstrating the use of humidifier disinfectant, disinfectant purchase receipts, any residual disinfectant, and the consistency of their statements. Exposure duration was estimated as cumulative disinfectant use hours from the questionnaire. Airborne disinfectant exposure intensity (µg/m(3)) was estimated based on the disinfectant volume (ml) and frequency added to the humidifier per day, disinfectant bulk level (µg/ml), the volume of the room (m(3)) with humidifier disinfectant, and the degree of ventilation. Overall, the distribution patterns of the intensity, duration, and cumulative exposure to humidifier disinfectants for the patient group were higher than those of the family group, especially for pregnant women and patients ≤6 years old. Further study is underway to evaluate the association between the disinfectant exposures estimated here with clinically diagnosed lung disease. PRACTICAL IMPLICATIONS: Retrospective exposure to household humidifier disinfectant as estimated here can be used to evaluate associations with clinically diagnosed lung disease due to the use of humidifier disinfectant in Korea. The framework, with modifications to account for dispersion and use patterns, can also be potentially adapted to assessment of other household chemical exposures.

Welding fume exposure and chronic obstructive pulmonary disease in welders.

BACKGROUND: Occupational exposure is estimated to contribute 15% to the burden of chronic obstructive pulmonary disease (COPD). Welding fumes are suspected to accelerate the decline of lung function and development of COPD. AIMS: To examine the relationship between welding fume exposure and COPD in Korean shipyard welders. METHODS: The study involved a group of male welders working at two shipyards who underwent an annual health examination in 2010. Subjects completed a questionnaire about smoking habits and occupational history and a pulmonary function test (PFT) was carried out with strict quality control measures. Welding fume exposure concentrations were estimated using 884 measurements taken between 2002 and 2009 in one of the shipyards. Multiple linear and logistic regression was employed to evaluate the association between cumulative fume exposure and lung function parameters, controlling for age, height and cigarette smoking. RESULTS: Two hundred and forty subjects participated, with a mean age of 48 and mean work duration of 15 years. The mean cumulative fume exposure was 7.7mg/m(3). The prevalence of COPD was 15%. FEV1 and FVC showed non-significant negative correlations with cumulative fume exposure. Odds ratios of COPD were significantly elevated for the middle (3.9; 95% CI 1.4-13.3) and high exposure groups (3.8; 95% CI 1.03-16.2) compared with the low fume exposure group. CONCLUSIONS: Our findings support an association between welding fume exposure and increased risk of COPD. Further prospective study is needed to investigate whether this is a causal relationship.

Standardization of automated analyses of oculomotor fixation and saccadic behaviors.

In an effort towards standardization, this paper evaluates the performance of five eye movement classification algorithms in terms of their assessment of oculomotor fixation and saccadic behavior. The results indicate that performance of these five commonly used algorithms vary dramatically even in the case of a simple stimulus evoked task using a single, common threshold value. The important contributions of this paper are: 1) evaluation and comparison of performance of five algorithms to classify specific oculomotor behavior 2) introduction and comparison of new standardized scores to provide more reliable classification performance 3) logic for a reasonable threshold value selection for any eye movement classification algorithm based on the standardized scores and 4) logic for establishing a criterion-based baseline for performance comparison between any eye movement classification algorithms. Proposed techniques enable efficient and objective clinical applications providing means to assure meaningful automated eye movement classification.

Clinical and immunologic findings of methylene diphenyl diisocyanate-induced occupational asthma in a car upholstery factory.

BACKGROUND: Although methylene diphenyl diisocyanate (MDI) is widely used in many industries, there have been few immunological studies of MDI-induced occupational asthma. OBJECTIVES: We investigated the effects of MDI exposure on the clinical and immunologic condition of workers in a single car upholstery factory. METHODS: Fifty-eight MDI-exposed workers were studied. Work-related lower-respiratory symptoms (WRRS) were identified using a questionnaire. Serum-specific IgE and IgG antibodies to MDI-human serum albumin conjugate were detected by ELISA. Atopy was evaluated using a skin prick test. MDI-induced occupational asthma was confirmed in the symptomatic workers with a positive result on an MDI-specific inhalation test. RESULTS: Thirteen (22.4%) of the subjects complained of WRRS. MDI-induced occupational asthma was confirmed in five (8.6%) of the workers, and occupational eosinophilic bronchitis was confirmed in two (3.5%). The prevalence of specific IgG antibodies (20.7%) was higher than that of specific IgE antibodies (8.6%). The prevalence of MDI-induced occupational asthma/eosinophilic bronchitis was strongly associated with the presence of both WRRS and serum-specific IgG antibodies to an MDI-human serum albumin conjugate (P<0.01, <0.05, respectively). CONCLUSION: These findings suggest that MDI could be a causative agent of occupational asthma among MDI-exposed workers. The prevalence of MDI-induced occupational asthma was 8.6%, and MDI-induced eosinophilic bronchitis was confirmed in two workers. The presence of work-related lower-respiratory symptoms and serum-specific IgG antibodies to an MDI-human serum albumin conjugate may be used to predict MDI-induced occupational asthma/eosinophilic bronchitis in MDI-exposed workers.

Histone deacetylase inhibitor apicidin downregulates DNA methyltransferase 1 expression and induces repressive histone modifications via recruitment of corepressor complex to promoter region in human cervix cancer cells.

Dysregulation of DNA methyltransferase (DNMT)1 expression is associated with cellular transformation, and inhibition of DNMT1 exerts antitumorigenic effects. Here, we report that DNMT1 abnormally expressed in HeLa cells is downregulated by a histone deacetylase (HDAC) inhibitor apicidin, which is correlated with induction of repressive histone modifications on the promoter site. Apicidin selectively represses the expression of DNMT1 among DNMTs in HeLa cells, independent of cell cycle arrest at G0/G1. Furthermore, apicidin causes a significant reduction in the recruitment of RNA polymerase II into the promoter. Chromatin immunoprecipitation analysis shows that even though apicidin causes global hyperacetylation of histone H3 and H4, localized deacetylation of histone H3 and H4 occurs at the E2F binding site, which is accompanied by the recruitment of pRB and the replacement of P/CAF with HDAC1 into the sites. In addition, K4-trimethylated H3 on nucleosomes associated with the transcriptional start site is depleted following apicidin treatment, whereas repressive markers, K9- and K27-trimethylation of H3 are enriched on the site. The downregulation of DNMT1 expression seems to require de novo protein synthesis, because the apicidin effect is antagonized by cycloheximide treatment. Moreover, knock down of DNMT1 with siRNA induces the apoptosis of HeLa cells, indicating that downregulation of DNMT1 might be a good strategy for therapeutics of human cervix cancer. Collectively, our findings will provide a mechanistic rationale for the use of HDAC inhibitors in cancer therapeutics.