Comparing individual-, family-, and community-level effects on the oral health of preschool children: a multilevel analysis of national survey data.

BACKGROUND: Early childhood is a critical stage for the prevention of dental caries. The prevalence of caries in preschool children is still high in Taiwan, where National Health Insurance covers 99% of the population. The effort to improve the oral health of preschool children should be based on conceptual model that encompasses more than individual-level factors. This study input nationwide survey data in a conceptual model to evaluate the effects of comprehensive factors related to the high prevalence of caries in preschool children. METHODS: This observation study examined factors related to the oral health of preschool children by employing a comprehensive multilevel model to analyse nationally representative data from the Taiwan Oral Health Survey of Preschool Children (TOHPC) 2017-2018. Individual-level, family-level and community-level contextual effects were evaluated through multilevel analysis in this study. The proportional change in variance (PCV) was used to compare the multilevel model with the null model and individual-level, family-level, and community-level context effects. RESULTS: The estimated deft index for preschool children was 1.34 (1.22-1.47) at age 3, 2.20 (2.08-2.32) at age 4, and 3.05 (2.93-3.18) at age 5. The overall prevalence of caries in preschool children in Taiwan was 34.27% (30.76%, 37.78%) at age 3, 51.67% (48.99%, 54.35%) at age 4, and 62.05% (59.66%, 64.44%) at age 5. The model that included the individual-, family-, and community-context levels exhibited the highest reduction of variance (PCV = 53.98%). The PCV was further reduced to 35.61% when only the level of accessibility to dental services for individuals, families, and the community was considered. For the model in which no community-context cofactors were considered and the model considering only the individual level, the PCVs were 20.37% and 5.52%, respectively. CONCLUSIONS: Our findings indicate the key components that affect oral health in preschool children and can serve as a reference for policy makers. The most notable finding of this study is that to improve the oral health of preschool children, community-level factors should be targeted. To rely solely on dentists for leading oral health education programs for children is impractical and inefficient. Training more professional oral health educators to provide additional community-based oral health promotion campaigns is critical. We suggest training more professional oral health educators to provide more community-based oral health promotion campaigns.

Oral health: The first step to sustainable development goal 3.

The 17 sustainable development goals (SDGs) were established by the United Nations Agenda 2030 plan of action to achieve peace, prosperity, and well-being for all by 2030. SDG 3 aims to ensure healthy lives and promote well-being for all at all ages. However, oral health is not specifically mentioned and targeted in SDG 3. Numerous studies have demonstrated a connection between oral health and general health. Oral disease and the common non-communicable diseases have the co-existing modifying risk factors. In addition, oral health is associated with social, economic, cultural, and environmental problems. By the implementation of oral health care, oral health promotion, and universal health coverage, these could not only be good for oral health but also benefit for general health and well-being. Taken together, oral health is the first step to SDG 3.

Initiating narrative medicine into dental education: Opportunity, change, and challenge.

Recently, the patient-centered and comprehensive dental treatment are emphasized as the same important competency as traditional clinical skill training in dental education. It is a silver lining to reorganize current dental education and redefine the role of dentistry to dentist, patient, and society. Narrative medicine has emerged as a variant from medical humanities and takes inspiration from philosophy, literature, poetry, art, ethics, and social sciences. Narrative medicine adds humanistic care with empathy and listening to patients in daily care. In this article, we introduce the definition of narrative medicine, the concept of narrative dentistry, implementation of narrative medicine into dental education, and challenges in initiating narrative dentistry. During the current COVID-19 pandemic, it also affords the opportunity to initiate narrative medicine into dental education, dentist could emerge to heal patient holistically, but not simply eliminate oral diseases.

IL-8 as a Potential Therapeutic Target for Periodontitis and Its Inhibition by Caffeic Acid Phenethyl Ester In Vitro.

Salivary levels of interleukin-8 (IL-8) are elevated in patients with periodontitis. Caffeic acid phenethyl ester (CAPE) improves the periodontal status in subjects. However, whether CAPE can reduce IL-8 expression is unclear. We collected saliva to determine proinflammatory cytokine levels and used subgingival calculus and surrounding tissues from patients with periodontitis for oral microbiota analysis via 16s ribosomal RNA gene sequencing. THP-1 cells were stimulated with sterile-filtered saliva from patients, and target gene/protein expression was assessed. IL-8 mRNA expression was analyzed in saliva-stimulated THP-1 cells treated with CAPE and the heme oxygenase-1 (HO-1) inhibitor tin-protoporphyrin (SnPP). In 72 symptomatic individuals, IL-8 was correlated with periodontal inflammation (bleeding on probing, r = 0.45; p < 0.001) and disease severity (bleeding on probing, r = 0.45; p < 0.001) but not with the four oral microbiota species tested. Reduced salivary IL-8 secretion was correlated with effective periodontitis treatment (r = 0.37, p = 0.0013). In THP-1 cells, saliva treatment induced high IL-8 expression and IKK2 and nuclear factor-κB (NF-κB) phosphorylation. However, the IKK inhibitor BMS-345541, NF-κB inhibitor BAY 11-7082, and CAPE attenuated saliva-induced IL-8 expression. CAPE induced HO-1 expression and inhibited IKK2, IκBα, and NF-κB phosphorylation. Blocking HO-1 decreased the anti-inflammatory activity of CAPE. The targeted suppression of IL-8 production using CAPE reduces inflammation and periodontitis.

Associations between the phenotype and genotype of MnSOD and catalase in periodontal disease.

BACKGROUND: Periodontal disease is an inflammatory disease in which pathogenic infections trigger a series of inflammatory responses and redox regulation. The hypothesis of this study was that a host's redox regulation, as modified by genetic polymorphisms, may affect periodontal disease activities (including the plaque index (PlI), bleeding on probing (BOP), and pocket depth (PD)) during periodontal therapy. METHODS: In total, 175 patients diagnosed with periodontitis were recruited from the Department of Periodontology, Taipei Medical University Hospital. Both saliva samples and clinical measurements (PlI, BOP, and PD) were taken at the baseline and at 1 month after completing treatment. Salivary manganese superoxide dismutase (MnSOD) and catalase, and corresponding genetic polymorphisms (MnSOD, T47C, rs4880 and Catalase, C-262 T, rs1001179) were determined. The extent of change (Δ) of MnSOD or catalase was calculated by subtracting the concentration after completing treatment from that at the baseline. RESULTS: Subjects who carried the Catalase CC genotype had significantly higher salivary MnSOD or catalase levels. The MnSOD genotype had a significant effect on the percentage of PDs of 4~9 mm (p = 0.02), and salivary ΔMnSOD had a significant effect on the PlI (p = 0.03). The Catalase genotype had a significant effect on the PlI (p = 0.01~0.04), but the effect was not found for the mean PlI or PD. There was a significant interaction between the MnSOD genotype and salivary ΔMnSOD on PDs of 4~9 mm. After adjusting for gender, years of schooling, smoking status, and alcohol consumption, subjects with ΔMnSOD of < 0 µg/ml or Δcatalase of < 0 µg/ml had significantly higher 5.58- or 5.17-fold responses to scaling and root planing treatment. CONCLUSIONS: The MnSOD T47C genotype interferes with the phenotype of salivary antioxidant level, alters MnSOD levels, and influences the PD recovery. MnSOD and catalase gene polymorphism associated with phenotype expression and susceptibility in periodontal root planing treatment responses.

Prophylactic supplement with melatonin successfully suppresses the pathogenesis of periodontitis through normalizing RANKL/OPG ratio and depressing the TLR4/MyD88 signaling pathway.

Periodontitis (PD) is an inflammatory disease characterized by gingival inflammation and resorption of alveolar bone. Impaired receptor activator of nuclear factor-kappa B ligand/osteoprotegerin (RANKL/OPG) signaling caused by enhanced production of pro-inflammatory cytokines plays an essential role in the pathogenesis of PD. Considering melatonin possesses significant anti-inflammatory property, this study aimed to determine whether prophylactic treatment with melatonin would effectively normalize RANKL/OPG signaling, depress toll-like receptor 4/myeloid differentiation factor 88 (TLR4/MyD88)-mediated pro-inflammatory cytokine activation, and successfully suppress the pathogenesis of PD. PD was induced in adult rats by placing the ligature at molar subgingival regions. Fourteen days before PD induction, 10, 50, or 100 mg/kg of melatonin was intraperitoneally injected for consecutive 28 days. Biochemical and enzyme-linked immunosorbent assay were used to detect TLR4/MyD88 activity, RANKL, OPG, interleukin 1ß, interleukin 6, and tumor necrosis factor-α levels, respectively. The extent of bone loss, bone mineral intensity, and calcium intensity was further evaluated by scanning electron microscopy, micro-computed tomography, and energy-dispersive X-ray spectroscopy. Results indicated that high RANKL/OPG ratio, TLR4/MyD88 activity, and pro-inflammatory cytokine levels were detected following PD. Impaired biochemical findings paralleled well with severe bone loss and reduced calcium intensity. However, in rats pretreated with melatonin, all above parameters were successfully returned to nearly normal levels with maximal change observed in rats receiving 100 mg/kg. As prophylactic treatment with melatonin effectively normalizes RANKL/OPG signaling by depressing TLR4/MyD88-mediated pro-inflammatory cytokine production, dietary supplement with melatonin may serve as an advanced strategy to strengthen oral health to counteract PD-induced destructive damage.

Static magnetic field attenuates lipopolysaccharide-induced inflammation in pulp cells by affecting cell membrane stability.

One of the causes of dental pulpitis is lipopolysaccharide- (LPS-) induced inflammatory response. Following pulp tissue inflammation, odontoblasts, dental pulp cells (DPCs), and dental pulp stem cells (DPSCs) will activate and repair damaged tissue to maintain homeostasis. However, when LPS infection is too serious, dental repair is impossible and disease may progress to irreversible pulpitis. Therefore, the aim of this study was to examine whether static magnetic field (SMF) can attenuate inflammatory response of dental pulp cells challenged with LPS. In methodology, dental pulp cells were isolated from extracted teeth. The population of DPSCs in the cultured DPCs was identified by phenotypes and multilineage differentiation. The effects of 0.4 T SMF on DPCs were observed through MTT assay and fluorescent anisotropy assay. Our results showed that the SMF exposure had no effect on surface markers or multilineage differentiation capability. However, SMF exposure increases cell viability by 15%. In addition, SMF increased cell membrane rigidity which is directly related to higher fluorescent anisotropy. In the LPS-challenged condition, DPCs treated with SMF demonstrated a higher tolerance to LPS-induced inflammatory response when compared to untreated controls. According to these results, we suggest that 0.4 T SMF attenuates LPS-induced inflammatory response to DPCs by changing cell membrane stability.

Change of scaling-induced proinflammatory cytokine on the clinical efficacy of periodontitis treatment.

Proinflammatory cytokines are key inflammatory mediators in periodontitis. This study aimed to investigate the relationship between proinflammatory cytokines in saliva and periodontal status. To investigate the usefulness of cytokines in the therapeutic approach for periodontal disease, the relationship between stimulated cytokine changes and the periodontitis treatment outcome was investigated in this study. Saliva was obtained from 22 patients diagnosed by dentists as having chronic periodontitis. The proinflammatory cytokine (interleukin-1α (IL-1α), interleukin-1ß (IL-1ß), interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor α (TNF-α), and tumor necrosis factor ß (TNF-ß)) levels were determined using a commercially available kit. The IL-1ß and IL-6 levels increased, whereas the TNF-ß levels decreased with the severity of periodontitis (4 mm pocket percentage). Poststimulation IL-1α, IL-6, and IL-8 levels were higher in patients who had an improved treatment outcome. The differences of IL-6 levels (cut point: 0.05 µg/g) yielded a sensitivity and specificity of 90.0% and 81.82%, respectively, for predicting the periodontitis treatment outcome. Among the proinflammatory cytokines, stimulated IL-6 was an excellent marker for predicting the periodontitis treatment outcome.

Methylomics analysis identifies epigenetically silenced genes and implies an activation of ß-catenin signaling in cervical cancer.

Using DNA methylation biomarkers in cancer detection is a potential direction in clinical testing. Some methylated genes have been proposed for cervical cancer detection; however, more reliable methylation markers are needed. To identify new hypermethylated genes in the discovery phase, we compared the methylome between a pool of DNA from normal cervical epithelium (n = 19) and a pool of DNA from cervical cancer tissues (n = 38) using a methylation bead array. We integrated the differentially methylated genes with public gene expression databases, which resulted in 91 candidate genes. Based on gene expression after demethylation treatment in cell lines, we confirmed 61 genes for further validation. In the validation phase, quantitative MSP and bisulfite pyrosequencing were used to examine their methylation level in an independent set of clinical samples. Fourteen genes, including ADRA1D, AJAP1, COL6A2, EDN3, EPO, HS3ST2, MAGI2, POU4F3, PTGDR, SOX8, SOX17, ST6GAL2, SYT9, and ZNF614, were significantly hypermethylated in CIN3+ lesions. The sensitivity, specificity, and accuracy of POU4F3 for detecting CIN3+ lesions were 0.88, 0.82, and 0.85, respectively. A bioinformatics function analysis revealed that AJAP1, EDN3, EPO, MAGI2, and SOX17 were potentially implicated in ß-catenin signaling, suggesting the epigenetic dysregulation of this signaling pathway during cervical cancer development. The concurrent methylation of multiple genes in cancers and in subsets of precancerous lesions suggests the presence of a driver of methylation phenotype in cervical carcinogenesis. Further validation of these new genes as biomarkers for cervical cancer screening in a larger population-based study is warranted.

DNA methylation of PAX1 as a biomarker for oral squamous cell carcinoma.

OBJECTIVES: DNA methylation has been shown to be a promising cancer biomarker. The aim of this study was to evaluate DNA methylation of three transcription factors, sex-determining region Y-box 1 (SOX1), paired box gene 1 (PAX1), and zinc-finger 582 (ZNF582), in detecting oral squamous cell carcinoma (OSCC). MATERIALS AND METHODS: A case-control study was conducted at Taipei Medical University Hospital in Taiwan with 31 cases of various oral cavity squamous cell carcinomas and 40 controls. Questionnaire data assessing environmental exposure, such as alcohol consumption, cigarette smoking, and betel nut chewing, were obtained from each participant. DNA from oral swabs were analyzed for methylation using quantitative methylation polymerase chain reaction with TaqMan probes. Methylation status was determined using a methylation index. RESULTS: Methylation levels of SOX1, PAX1, and ZNF582 were significantly higher in cancer patients (p = 0.02, p = 0.02, and p = 0.03, respectively). Patients with highly methylated SOX1, PAX1, and ZNF582 had an increased cancer risk with odds ratios (ORs) of 16.50 (95 % CI = 2.85-96.65), 60.57 (95 % CI = 5.85-629.94), and 5.07 (95 % CI = 1.08-23.76), respectively. Area under the curve (AUC) values were 0.85, 0.78, and 0.78 for PAX1, SOX1, and ZNF582, respectively. When stratified based on environmental exposure, the AUC of PAX1 methylation (PAX1 (m) ) was 0.94 in environmental exposure-naïve subjects and 0.85 for SOX1 methylation in subjects who chewed betel nut. In general, the sensitivity and specificity of PAX1 (m) were 87 and 80 % for OSCC detection. The sensitivity of PAX1 (m) in subjects who chewed betel nut was 83 %, with a specificity of 75 %. CONCLUSIONS: Testing PAX1 DNA methylation using oral swabs is a promising method for oral cancer detection. Combined assessments regarding betel nut consumption and DNA methylation can improve OSCC screening. CLINICAL RELEVANCE: The double E (environmental and epigenetic) assessment is a potential strategy in OSCC screening.

Sanguis draconis, a dragon's blood resin, attenuates high glucose-induced oxidative stress and endothelial dysfunction in human umbilical vein endothelial cells.

Hyperglycaemia, a characteristic feature of diabetes mellitus, induces endothelial dysfunction and vascular complications by limiting the proliferative potential of these cells. Here we aimed to investigate the effect of an ethanolic extract of Sanguis draconis (SD), a kind of dragon's blood resin that is obtained from Daemonorops draco (Palmae), on human umbilical vein endothelial cells (HUVEC) under high-glucose (HG) stimulation and its underlying mechanism. Concentration-dependent (0-50 µg/mL) assessment of cell viability showed that SD does not affect cell viability with a similar trend up to 48 h. Remarkably, SD (10-50 µg/mL) significantly attenuated the high-glucose (25 and 50 mM) induced cell toxicity in a concentration-dependent manner. SD inhibited high glucose-induced nitrite (NO) and lipid peroxidation (MDA) production and reactive oxygen species (ROS) formation in HUVEC. Western blot analysis revealed that SD treatments abolished HG-induced phosphorylation of extracellular signal-regulated kinase 1/2 (ERK 1/2), nuclear transcription factor, κB (NF-κB), VCAM-1, and E-selectin, and it also blocked the breakdown of PARP-116 kDa protein in a dose-dependent manner. Furthermore, we found that SD increased the expression of Bcl-2 and decreased Bax protein expression in HG-stimulated HUVEC. Thus, these results of this study demonstrate for the first time that SD inhibits glucose induced oxidative stress and vascular inflammation in HUVEC by inhibiting the ERK/NF-κB/PARP-1/Bax signaling cascade followed by suppressing the activation of VCAM-1 and E-selectin. These data suggest that SD may have a therapeutic potential in vascular inflammation due to the decreased levels of oxidative stress, apoptosis, and PARP-1 activation.

Scaling-stimulated salivary antioxidant changes and oral-health behavior in an evaluation of periodontal treatment outcomes.

AIM: Our goal was to investigate associations among scaling-stimulated changes in salivary antioxidants, oral-health-related behaviors and attitudes, and periodontal treatment outcomes. MATERIALS AND METHODS: Thirty periodontitis patients with at least 6 pockets with pocket depths of >5 mm and more than 16 functional teeth were enrolled in the study. Patients were divided into three groups: an abandoned group (AB group), a nonprogress outcome group (NP group), and an effective treatment group (ET group). Nonstimulated saliva was collected before and after scaling were received to determine superoxide dismutase (SOD) and the total antioxidant capacity (TAOC). RESULTS: Salivary SOD following scaling significantly increased from 83.09 to 194.30 U/g protein in patients who had irregular dental visit patterns (<1 visit per year). After scaling, the TAOC was significantly higher in patients who had regular dental visits than in patients who had irregular dental visits (3.52 versus 0.70 mmole/g protein, P < 0.01). The scaling-stimulated increase in SOD was related to a higher severity of periodontitis in the NP group, while the scaling-stimulated increase in the TAOC was inversely related to the severity of periodontitis in the AB group. CONCLUSIONS: These results demonstrate the importance of scaling-stimulated salivary antioxidants as prognostic biomarkers of periodontal treatment.

Effect of Antrodia camphorata on inflammatory arterial thrombosis-mediated platelet activation: the pivotal role of protein kinase C.

Antrodia camphorata is a rare Taiwanese medicinal mushroom. Antrodia camphorata extract has been reported to exhibit antioxidant, anti-inflammation, antimetastasis, and anticancer activities and plays a role in liver fibrosis, vasorelaxation, and immunomodulation. Critical vascular inflammation leads to vascular dysfunction and cardiovascular diseases, including abdominal aortic aneurysms, hypertension, and atherosclerosis. Platelet activation plays a crucial role in intravascular thrombosis, which is involved in a wide variety of cardiovascular diseases. However, the effect of Antrodia camphorata on platelet activation remains unclear. We examined the effects of Antrodia camphorata on platelet activation. In the present study, Antrodia camphorata treatment (56-224 µg/mL) inhibited platelet aggregation induced by collagen, but not U46619, an analogue of thromboxane A2, thrombin, and arachidonic acid. Antrodia camphorata inhibited collagen-induced calcium (Ca(2+)) mobilization and phosphorylation of protein kinase C (PKC) and Akt. In addition, Antrodia camphorata significantly reduced the aggregation and phosphorylation of PKC in phorbol-12, 13-dibutyrate (PDBu) activated platelets. In conclusion, Antrodia camphorata may inhibit platelet activation by inhibiting of Ca(2+) and PKC cascade and the Akt pathway. Our study suggests that Antrodia camphorata may be a potential therapeutic agent for preventing or treating thromboembolic disorders.

A static magnetic field attenuates lipopolysaccharide-induced neuro-inflammatory response via IL-6-mediated pathway.

An effective method for controlling brain damage and neurodegeneration caused by inflammation remains elusive. Down-expression of the lipopolysaccharide (LPS)-induced inflammatory cytokines resulting in endotoxin tolerance is reported as an alternative anti-infection treatment. Nonetheless, because the dosage and action site are hard to control, endotoxin tolerance caused by low-dose LPS injection in brain tissue may induce side effects. The aim of this study was to test the hypothesis that static magnetic fields (SMF) stimulate endotoxin tolerance in brain tissue. In this study, survival rate and pathological changes in brain tissues of LPS-challenged mice were examined with and without SMF treatment. In addition, the effects of SMF exposure on growth rate and cytokine expression of LPS-challenged BV-2 microglia cells were monitored. Our results showed that SMF pre-exposure had positive effects on the survival rate and histological outcomes of LPS-treated mice. Furthermore, SMF exposure significantly decreased IL-6 expression in BV-2 cells (p < 0.05) by a phenomenon similar to endotoxin tolerance. We suggest that SMF has potential as an alternative simulation source for controlling LPS-induced excess neuro-inflammatory response.

Polymorphism of inflammatory genes and arsenic methylation capacity are associated with urothelial carcinoma.

Chronic exposure to arsenic can generate reactive oxidative species, which can induce certain proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and interleukin-8 (IL-8). TNF-α, IL-6 and IL-8 have been shown to be involved in the development and progression of various cancers, including bladder cancer. This study aimed to investigate the joint effect of the polymorphism of TNF-α -308 G/A, IL-6 -174 G/C, IL-8 -251 T/A and urinary arsenic profiles on urothelial carcinoma (UC) risk. This study evaluated 300 pathologically-confirmed cases of UC and 594 cancer-free controls. Urinary arsenic species were detected using high-performance liquid chromatography-linked hydride generator and atomic absorption spectrometry. The polymorphism of TNF-α -308 G/A, IL-6 -174 G/C and IL-8 -251 T/A was determined using polymerase chain reaction-restriction fragment length polymorphism. The joint effects on UC risk were estimated by odds ratios and 95% confidence intervals using unconditional logistic regression. We found that the TNF-α -308 A/A and IL-8 -251 T/T polymorphisms were significantly associated with UC. Moreover, significant dose-response joint effect of TNF-α -308 A/A or IL-8 -251 T/T genotypes and arsenic methylation indices were seen to affect UC risk. The present results also showed a significant increase in UC risk in subjects with the IL-8 -251 T/T genotype for each SD increase in urinary total arsenic and MMA%. In contrast, a significant decrease in UC risk was found in subjects who carried the IL-8 -251 T/T genotype for each SD increase in DMA%.

Urinary arsenic profiles and the risks of cancer mortality: a population-based 20-year follow-up study in arseniasis-endemic areas in Taiwan.

Few studies investigated the association between chronic arsenic exposure and the mortality of cancers by estimating individual urinary arsenic methylation profiles. Therefore, we compared with the general population in Taiwan to calculate the standardized mortality ratio (SMR) in arseniasis-endemic area of Taiwan from 1996 to 2010 and evaluated the dose-response relationships between environmental arsenic exposure indices or urinary arsenic profiles and the mortality of cause-specific cancer. A cohort of 1563 residents was conducted and collected their urine sample and information regarding arsenic exposure from a questionnaire. All-cause death was identified using the National Death Registry of Taiwan. Urinary arsenic profiles were measured using high performance liquid chromatography-hydride generator-atomic absorption spectrometry. We used Cox proportional hazard models to evaluate the mortality risks. In results, 193 all-site cancer deaths, and 29, 71, 43 deaths respectively for liver, lung and bladder cancers were ascertained. The SMRs were significantly high in arseniasis-endemic areas for liver, lung, and bladder cancers. People with high urinary InAs% or low DMA% or low secondary methylation index (SMI) were the most likely to suffer bladder cancer after adjusting other risk factors. Even stopping exposure to arsenic from the artesian well water, the mortality rates of the residents were higher than general population. Finally, urinary InAs%, DMA% and SMI could be the potential biomarkers to predict the mortality risk of bladder cancer.

Environmental tobacco smoke and arsenic methylation capacity are associated with urothelial carcinoma.

BACKGROUND/PURPOSE: Cigarette smoking, exposure to secondhand smoke, and arsenic exposure are well known risk factors for developing urothelial carcinoma (UC). We investigated the combined effects of cigarette smoking, exposure to secondhand smoke, and the presence of urinary total arsenic on the risk of developing UC. METHODS: We conducted a hospital-based, case-control study involving 261 UC patients and 672 cancer-free control individuals between September 2002 and May 2009. RESULTS: Individuals who had smoked <100 cigarettes in their lifetime (never smokers) and had a high urinary total arsenic level (≥15.40 µg/g creatinine), and those who had smoked >100 cigarettes in their lifetime (ever smokers) and had a high urinary total arsenic level, had increased risks of developing UC (3.20-fold and 6.45-fold greater), respectively, compared to individuals who were never smokers and had a low urinary total arsenic level. Individuals who had high urinary total arsenic levels and had been exposed to secondhand smoke, and individuals with high urinary arsenic levels who had not been exposed to secondhand smoke, had increased chances (2.71-fold and 5.00-fold greater, respectively) of developing UC, compared to individuals who were not exposed to secondhand smoke and had low urinary total arsenic levels. Ever smokers who had been exposed to secondhand smoke and had a high urinary total arsenic level had the greatest increased risk for developing UC (10.82-fold greater). CONCLUSION: Individuals in a Taiwanese population who smoked cigarettes, were exposed to secondhand smoke, and a high urinary total arsenic level, had a significant risk for developing UC.

Heat acclimation decreased oxidative DNA damage resulting from exposure to high heat in an occupational setting.

Heat acclimation is a physiologically and biochemically adapted process when species transition from one environmental temperature to one of the increased temperature. There is very limited epidemiological evidence on the heat-related impacts during exposure to extremely high heat in an occupational environment. This study sought to identify a potential biomarker of heat acclimation and the burden of heat on the body. The aim of this study was to elucidate oxidative DNA damage and heat acclimation through a self-comparison study design in navy boiler tenders, subjects exposed to extremely high heat in an occupational setting. Fifty-eight male soldiers who work in a boiler room were recruited for this study. The subjects were initially assessed with a health examination and body composition assessment before sailing. In order to compare the within-subject differences before and after heat exposure, the index-related heat exposure was collected before and after a routine 5-h work shift and 7-day sailing. Urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG), a useful marker of oxidative DNA damage was the measurement by liquid chromatography/tandem mass spectrometry. The median of the change in urinary 8-OHdG was 0.78 µg/g creatinine, as the urinary 8-OHdG after sailing was significantly higher than before sailing (p < 0.01). The urinary 8-OHdG was significantly decreased in heat-acclimated boiler tenders. Oxidative DNA damage was significantly decreased in heat-acclimated subjects. Urinary 8-OHdG can be used as a biomarker to assess the effect of heat stress as a result of occupational exposure to extremely high heat conditions.