On the Association Between Demographic Structural Change and the Effectiveness of Nurse Staffing Policy for Inpatient Care: Evidence from Taiwan.

Purpose: This study investigates the influence of demographic changes on the effectiveness of hospital nurse staffing policy, measured by the cumulative response of inpatient care quality to adjustments in hospital nurse staffing levels in Taiwan. Methods: The research design utilized in this study aligns with the observational time-series methodology, and a total of 99 monthly time-series observations were collected from multiple databases administered by the Taiwan government over the period from January 2015 to March 2023. Specifically, the time-varying parameter vector autoregressive and autoregressive distributed lag models were employed to investigate the association between age distribution and nurse staffing policy effectiveness. Results: The time-varying impulse responses of the unplanned 14-day readmission rate after discharge to changes in nurse staffing levels indicate a positive association between patient-to-nurse ratios and unplanned 14-day readmission rates across various types of hospitals. Nevertheless, the effectiveness of hospitals' nurse staffing policy is observed to diminish with population aging, particularly evident in medical centers and regional hospitals. Conclusion: Policymakers should establish lower mandated patient-to-nurse ratios, grounded in practical nurse workforce planning, to address the needs of an aging society and enhance inpatient care quality through improved nurse staffing in hospitals.

Hibifolin protected pro-inflammatory response and oxidative stress in LPS-induced acute lung injury through antioxidative enzymes and the AMPK2/Nrf-2 pathway.

ALI is a grave medical ailment that manifests as abrupt inflammation of the lungs and diminished oxygen levels. It poses a considerable challenge to the medical fraternity, with elevated rates of morbidity and mortality. Our research endeavors to investigate the potential of hibifolin, a flavonoid glucuronide, imbued with potent antioxidant properties, and its molecular mechanism to combat LPS-induced ALI in mice. The study utilized ICR mice to create an ALI model induced by LPS. Prior to LPS administration, hibifolin was given at 10, 30, or 50 mg/kg, or dexamethasone was given at 1 mg/kg to assess its preventative impact. Changes in lung tissue, pulmonary edema, and lipid peroxidation were analyzed using H&E stain assay, lung wet/dry ratio assay, and MDA formation assay, respectively. Activity assay kits were used to measure MPO activity and antioxidative enzymes (SOD, CAT, GPx) activity in the lungs. Western blot assay was used to determine the phosphorylation of Nrf-2 and AMPK2 in the lungs. Hibifolin demonstrated a concentration-dependent improvement in LPS-induced histopathologic pulmonary changes. This treatment notably mitigated pulmonary edema, lipid peroxidation, and MPO activity in ALI mice. Additionally, hibifolin successfully restored antioxidative enzyme activity in the lungs of ALI mice. Moreover, hibifolin effectively promoted Nrf-2 phosphorylation and reinstated AMPK2 phosphorylation in the lungs of ALI mice. The results indicate that hibifolin could effectively alleviate the pathophysiological impact of LPS-induced ALI. This is likely due to its antioxidative properties, which help to restore antioxidative enzyme activity and activate the AMPK2/Nrf2 pathway. These findings are valuable in terms of enhancing our knowledge of ALI treatment and pave the way for further investigation into hibifolin as a potential therapeutic option for lung injuries.

The association between smoking cessation and lifestyle/genetic variant rs6265 among the adult population in Taiwan.

Recent studies showed significant associations between socio-demographic, lifestyle factors, polymorphic variant rs6265, and smoking cessation behaviours. We examined rs6265 TT, TC and CC genotypes and their association with socio-demographic and other variables, including mental health status, drinking, exercise, and smoking behaviour among Taiwanese adults. Data on rs6265 were retrieved from the Taiwan Biobank, which contained genetic data collected between 2008 to 2019 from 20,584 participants (aged 30-70 years). Participants who smoked for more than 6 months prior to enrolment were categorized as smokers. If they had smoked and later quit for more than 6 months, they were classified as former smokers. Information regarding drinking, exercise, depression, and bipolar disorder were obtained through questionnaires and were categorized as either as affirmative (yes) or negative (no) responses. In contrast to previous studies, we found that the association between the polymorphism rs6265 and smoking behaviour was not significant (P-value = 0.8753). Males with lower education levels, young persons, and alcohol drinkers showed significant smoking behaviours (P-value < .0001). This population-based study indicates that rs6265 has no significant correlations with smoking cessation behaviour among adults in Taiwan.

Allergic rhinitis children with obesity are more vulnerable to air pollution: a cross sectional study.

The association between air pollution, allergic rhinitis (AR), and obesity has not been studied. From 2007 to 2011, 52 obese and 152 non-obese children (7-17 years old) with AR were recruited. Pediatric-Rhinoconjunctivitis-Quality-of-Life Questionnaire (PRQLQ) and nasal peak expiratory flow (NPEF) were tested. Association between the scores and rates of the two tests and mean air pollutant concentrations within 7 days before the tests were compared. When exposed to higher concentrations of CO, PM10, and PM2.5, the rates of worse nasal discomfort were 39.4%, 44.4% and 39.3% in obese children; and 18.0%, 21.9% and 19.7% in non-obese children, respectively. Compare to non-obese children, the rates in obese children were higher for CO (odds ratio (OR) 3.54, 95% confidence interval (CI) 1.15 ~ 10.92); PM10 (OR 3.26, 95% CI 1.01 ~ 10.57) and PM2.5 (OR 3.30; 95% CI 1.03 ~ 10.54). In obese children, correlations between higher concentrations of CO, PM10, PM2.5 and higher nasal discomfort (higher PRQLQ); and correlations between higher concentrations of CO, PM10, PM2.5, NMHC (non-methane hydrocarbon) and higher nasal mucosa inflammation (lower NPEF) were noted. Obesity negatively affected AR severity when AR children experienced higher concentrations of CO, PM10, and PM2.5. Increased nasal inflammation induced by air pollutants might be the underlying mechanism.

Relationship between periodontal disease and dizziness in Taiwanese adults: A nationwide population-based cohort study.

Periodontal disease is often neglected and overlooking its initial symptoms can lead to tooth loss and systemic diseases. Patients with otitis media are at high risk of vestibular and balance dysfunction, consequently, and vertigo. Vertigo and dizziness are conditions with high reported incidences; they worsen with age and can burden health systems. The present study investigated whether periodontal disease causes dizziness. Research data covering 2008 through 2013 were retrieved from the National Health Insurance Research Database of Taiwan. Patients who were newly diagnosed as having periodontal disease or dizziness after at least 1 hospital admission or 3 outpatient visits were enrolled as participants. For our controls, we randomly selected individuals without periodontal disease who were sex- and age-matched with the investigated participants. In total, we enrolled 445 patients with periodontal disease and 1780 controls. The Kaplan-Meier curve indicated that the cumulative incidence of dizziness was significantly higher among the patients with periodontal disease relative to the controls. After adjustment for sex, age, income level, urbanization level, month of onset, and comorbidities, Cox proportional-hazards analysis revealed that patients with periodontal disease had an increased risk of dizziness (hazard ratio [HR]: 1.306, 95% confidence interval (CI): 1.155, 1.475). Compared with the controls, the risk of dizziness among patients with periodontal disease was higher for both female (HR: 1.439, 95%: 1.203, 1.720) and male patients (HR: 1.284, 95%: 1.123, 1.468); this risk was higher even when January (HR: 1.302, 95% CI: 1.145, 1.480), February (HR: 1.337, 95% CI: 1.178, 1.518), or March was excluded (HR: 1.308, 95% CI: 1.151, 1.487) and for patients without Ménière disease. Therefore, periodontal disease is not only a risk factor for dizziness but also an independent risk factor for dizziness. Future studies could clarify the mechanisms linking periodontal disease to dizziness.

Cytotoxicity and Apoptotic Mechanism of 2-Hydroxyethyl Methacrylate via Genotoxicity and the Mitochondrial-Dependent Intrinsic Caspase Pathway and Intracellular Reactive Oxygen Species Accumulation in Macrophages.

Macrophages are mainly active cells of the immune system and play a role in the defense of pathogens. However, the overactivation of macrophages by fatal pathogens can result in toxic responses. 2-hydroxyethyl methacrylate (HEMA), which is a hydrophilic monomer, is used in dental adhesive reagents and composite resins as well as biocompatible hydrogels. The mechanisms underlying the genotoxicity engendered by HEMA-induced apoptosis that leads to cytotoxicity remain unclear. Accordingly, this study was conducted to clarify such mechanisms. The results showed that HEMA induced cell toxicity in RAW264.7 macrophages depending on the concentration. A higher HEMA concentration was associated with a higher level of apoptosis and genotoxicity. Moreover, HEMA induced a concentration-dependent increase in mitochondrial dysfunction and the intrinsic caspase pathway, including the activation of caspase-3 and caspase-9. HEMA was also found to upregulate intracellular reactive oxygen species generation and to decrease the activity of antioxidant enzymes, including superoxide dismutase and catalase. Taken together, the mitochondrial-dependent intrinsic caspase pathway and intracellular reactive oxygen species accumulation were found to mediate HEMA-induced genotoxicity and apoptosis, leading to cytotoxicity in RAW264.7 macrophages.

Depletion of miR-155 hinders the myofibroblast activities and reactive oxygen species generation in oral submucous fibrosis.

BACKGROUND/PURPOSE: Emerging evidence suggests the significance of microRNA-155 (miR-155) in fibrogenesis and oxidative stress accumulation, but its function in oral submucous fibrosis (OSF) has not been investigated. In this study, we assessed the expression of miR-155 and its effects on the maintenance of myofibroblast activation. METHODS: qRT-PCR was conducted to assess the expression of miR-155 in OSF tissues and fibrotic buccal mucosal fibroblasts (fBMFs) derived from OSF samples. Collagen gel contraction, migration, and invasion capabilities were examined in fBMFs. DCFDA ROS assay was used to examine ROS generation. A luciferase reporter assay was carried out to verify the relationship between miR-155 and its potential target RPTOR. RESULTS: We showed that the expression of miR-155 was aberrantly upregulated in OSF specimens and fBMFs. Inhibition of miR-155 ameliorated various myofibroblast activities, including collagen gel contraction, migration, and invasion abilities as well as ROS production. Results from the luciferase reporter assay demonstrated that miR-155 directly interacted with its target RPTOR. CONCLUSION: Taken together, these findings indicate that miR-155 is implicated in the pathogenesis of oxidative stress-associated OSF, possibly through the regulation of RPTOR.

3-Bromofluoranthene-induced cardiotoxicity of zebrafish and apoptosis in the vascular endothelial cells via intrinsic and extrinsic caspase-dependent pathways.

Fluoranthene, a high-molecular-weight polycyclic aromatic hydrocarbon (PAH), is widely present in air pollutants, including fine inhalable particulate matter. 3-Bromofluoranthene (3-BrFlu), which is a brominated fluoranthene and halogenated PAH, is generated from waste combustion, metallurgical processes, cement production, e-waste dismantling, and photoreaction. Vascular endothelial cells have key functions in the homeostasis and the development of the cardiovascular system. The zebrafish model has been widely employed to study cardiotoxicity and embryotoxicity. However, no evidence has indicated that 3-BrFlu induces cytotoxicity in vascular endothelial cells, or cardiotoxicity and embryotoxicity in zebrafish. In this study, 3-BrFlu induced concentration-dependent changes in embryo- and cardiotoxicity. Cytotoxicity was also induced by 3-BrFlu in a concentration-dependent manner through apoptosis and necrosis in vascular endothelial cells, SVEC4-10 cells. The activities of caspase-3, -8, and -9 were induced by 3-BrFlu via an intrinsic pathway constituting Bcl-2 downregulation, Bad upregulation, and mitochondrial dysfunction; the extrinsic pathway included the expression of death receptors, including tumour necrosis factor α and Fas receptors. These results indicated that 3-BrFlu caused cardio- and embryotoxicity in zebrafish through vascular endothelial cells cytotoxicity resulting from caspase-dependent apoptosis through intrinsic and extrinsic pathways.

Social Participation and Survival in Widowed Persons: Results of the Taiwan Longitudinal Study on Aging.

It has been considered that widowed persons have a higher risk of death. This study intended to explore whether social participation could improve this trend. A longitudinal study database was constructed to explore the trend of survival and its change with social participation in widowed persons. The Taiwan Longitudinal Study on Aging (TLSA), based on four consecutive waves of longitudinal follow-up data in 1999, 2003, 2007, and 2011 was linked with the National Death Registry from 1999 through 2012. In total, there were 1417 widowed persons and 4500 nonwidowed persons included in this study, excluding divorced and never-married people. The survival trend analysis was carried out with social participation as the main predictive factor stratified for comparative analysis. Our results showed that the widowed were older than the nonwidowed, were female-dominant, had a lower education level, were more economically stressed, and were less likely to engage in regular exercise, and thus showed generally poorer health; for example, being more vulnerable to having chronic diseases, disability with the Activities of Daily Living (ADL), cognitive impairment with the Short Portable Mental State Questionnaire (SPMSQ), and depression with The Center for Epidemiological Studies-Depression (CES-D). The death risk of the widowed was significantly higher than that of the nonwidowed, but the death trend for those with social participation was significantly lower than that of their counterparts in both the widowed and nonwidowed. After matching with gender and age for widowed persons, the widowed with social participation had a significantly lower risk of death (adjusted hazard ratio (HR), 0.83; 95% confidence interval (CI), 0.71-0.98) compared to the widowed without social participation. It was concluded that social participation can improve the death risk for the widowed, and it is worthily included in health promotion plans and social welfare services for widowed persons.

Association of Metabolic Syndrome with Aerobic Exercise and LPL rs3779788 Polymorphism in Taiwan Biobank Individuals.

PURPOSE: The Lipoprotein lipase (LPL) gene is a significant contributor to dyslipidemia. It has shown associations with several conditions including atherosclerosis, obesity, and metabolic syndrome (MetS). We assessed the interactive association between MetS and rs3779788 of the LPL gene based on aerobic exercise. MATERIALS AND METHODS: Data were available for 7532 Taiwan Biobank (TWB) participants recruited between 2008 and 2016. We used multiple logistic regression to determine the odds ratios (OR) for MetS and their 95% confident intervals (C.I.). Potential variables included LPL rs3779788, aerobic exercise, sex, age, education, marital status, body mass index (BMI), smoking, alcohol consumption, midnight snacking, vegetarian diet, coffee, dietary fat, and tea drinking. RESULTS: Aerobic exercise was protective against MetS (OR, 0.858; 95% C.I., 0.743-0.991). Compared to CC/CT genotype, the OR for developing MetS was 0.875, (95% C.I., 0.571-1.341) in TT individuals. The test for interaction was significant for the rs3779788 variant and aerobic exercise (p = 0.0484). In our group analyses, the OR for MetS was 0.841 (95% C.I., 0.727-0.974) in CC/CT and 4.076 (95% C.I., 1.158-14.346) in TT individuals who did aerobic exercise compared to those who did not. CONCLUSION: Our study indicated that aerobic exercise improved metabolic syndrome in Taiwanese adults with rs3779788 CC/CT genotype relative to those with TT genotype.

1-Nitropyrene Induced Reactive Oxygen Species-Mediated Apoptosis in Macrophages through AIF Nuclear Translocation and AMPK/Nrf-2/HO-1 Pathway Activation.

1-Nitropyrene (1-NP), one of the most abundant nitropolycyclic aromatic hydrocarbons (nitro-PAHs), is generated from the incomplete combustion of carbonaceous organic compounds. 1-NP is a specific marker of diesel exhaust and is an environmental pollutant and a probable carcinogen. Macrophages participate in immune defense against the invasive pathogens in heart, lung, and kidney infection diseases. However, no evidence has indicated that 1-NP induces apoptosis in macrophages. In the present study, 1-NP was found to induce concentration-dependent changes in various cellular functions of RAW264.7 macrophages including cell viability reduction; apoptosis generation; mitochondrial dysfunction; apoptosis-inducing factor (AIF) nuclear translocation; intracellular ROS generation; activation of the AMPK/Nrf-2/HO-1 pathway; changes in the expression of BCL-2 family proteins; and depletion of antioxidative enzymes (AOE), such as glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD) These results indicate that 1-NP induced apoptosis in macrophages through AIF nuclear translocation and ROS generation due to mitochondrial dysfunction and to the depletion of AOE from the activation of the AMPK/Nrf-2/HO-1 pathway.

Genotoxic effects of 1-nitropyrene in macrophages are mediated through a p53-dependent pathway involving cytochrome c release, caspase activation, and PARP-1 cleavage.

Genotoxic stress from environmental pollutants plays a critical role in cytotoxicity. The most abundant nitro-polycyclic aromatic hydrocarbon in environmental pollutants, 1-nitropyrene (1-NP), is generated during fossil fuel, diesel, and biomass combustion under sunlight. Macrophages, the key regulators of the innate immune system, provide the first line of defense against pathogens. The toxic effects of 1-NP on macrophages remain unclear. Through a lactate dehydrogenase assay, we measured the cytotoxicity induced by 1-NP. Our results revealed that 1-NP induced genotoxicity also named DNA damage, including micronucleus formation and DNA strand breaks, in a concentration-dependent manner. Furthermore, 1-NP induced p53 phosphorylation and nuclear accumulation; mitochondrial cytochrome c release; caspase-3 and -9 activation and cleavage; and poly (ADP-ribose) polymerase-1 (PARP-1) cleavage in a concentration-dependent manner. Pretreatment with the PARP inhibitor, 3-aminobenzamide, significantly reduced cytotoxicity, genotoxicity, and PARP-1 cleavage induced by 1-NP. Pretreatment with the caspase-3 inhibitor, z-DEVD-fmk, significantly reduced cytotoxicity, genotoxicity, PARP-1 cleavage, and caspase 3 activation induced by 1-NP. Pretreatment with the p53 inhibitor, pifithrin-α, significantly reduced cytotoxicity, genotoxicity, PARP-1 cleavage, caspase 3 activation, and p53 phosphorylation induced by 1-NP. We propose that cytotoxicity and genotoxicity induced by 1-NP by PARP-1 cleavage via caspase-3 and -9 activation through cytochrome c release from mitochondria and its upstream p53-dependent pathway in macrophages.

Protective Effects of Kirenol against Lipopolysaccharide-Induced Acute Lung Injury through the Modulation of the Proinflammatory NFκB Pathway and the AMPK2-/Nrf2-Mediated HO-1/AOE Pathway.

Acute lung injury (ALI) is an acute and life-threatening inflammatory disease of the lung parenchyma that is associated with high mortality worldwide. No therapeutic strategies have been developed for the mitigation of the proinflammatory response that characterizes ALI. Kirenol has anti-inflammatory, antiarthritic, and immunoregulatory effects. In the present study, we investigated the protective effects of kirenol against lipopolysaccharides (LPS)-induced ALI in mice. Kirenol reduced the LPS-induced histopathology changes involving edema and thickening of the interstitial or alveolar walls, infiltration of leukocytes, formation of hyaline membrane. Pretreatment with kirenol reduced leukocytes infiltration in bronchoalveolar lavage fluid (BALF), the alveolar-capillary barrier disruption and lipid peroxidation in lung tissues induced by LPS. Kirenol significantly inhibited the secretion of cytokines, IL-1ß, IL6, and TNFα, into the BALF of the mice with LPS-induced ALI through NFκB activation. Moreover, kirenol attenuated the downregulation of the antioxidant enzymes, superoxide dismutase, glutathione peroxidase, and catalase that was induced by LPS. HO-1 expression and the phosphorylation of Nrf2 and AMPK2 were also induced by kirenol. The results indicate that kirenol can be developed as a treatment strategy for ALI, and its effects are induced through the inhibition of the NF-κB proinflammatory pathway and promotion of AMPK2/Nrf2-mediated HO-1 and antioxidant enzymes (AOE) activation.

Association Between PM2.5 Exposure Level and Primary Open-Angle Glaucoma in Taiwanese Adults: A Nested Case-Control Study.

Primary open-angle glaucoma (POAG) is the most common type of glaucoma. However, little is known about POAG in adults and exposure to air pollution. The current study aims to investigate whether exposure to particulate matter with a mass median aerodynamic diameter of ≤2.5 µm (PM2.5) is associated with POAG diagnosis. Patient data were obtained from the Longitudinal Health Insurance Database 2010 (LHID2010) of Taiwan for the 2008-2013 period. PM2.5 concentration data, collected from the Ambient Air Quality Monitoring Network established by the Environmental Protection Administration of Taiwan, were categorized into four groups according to World Health Organization (WHO) exposure standards for PM2.5. We estimated the odds ratios (ORs) and 95% CIs for risk factors for POAG with logistic regression. The OR of per WHO standard level increase was 1.193 (95% CI 1.050-1.356). Compared with the normal level, the OR of WHO 2.0 level was 1.668 (95% CI 1.045-2.663, P < 0.05). After excluding confounding risk factors for POAG in this study, we determined that increased PM2.5 exposure is related to POAG risk (ORs > 1, P < 0.05). In this study, PM2.5 was an independent factor associated with open-angle glaucoma. Further research is required to better understand the mechanisms connecting PM2.5 and open-angle glaucoma.

Rutin-protected BisGMA-induced cytotoxicity, genotoxicity, and apoptosis in macrophages through the reduction of the mitochondrial apoptotic pathway and induction of antioxidant enzymes.

Bisphenol-A-glycidyldimethacrylate (BisGMA) is a resin monomer frequently used in dentin restorative treatments. The leakage of BisGMA monomer from BisGMA-based polymeric resins can lead to cytotoxicity in macrophages. Rutin has various beneficial bioeffects, including antioxidation and antiinflammation. In this study, we found that pretreatment of RAW264.7 macrophages with rutin-inhibited cytotoxicity induced by BisGMA in a concentration-dependent manner. BisGMA-induced apoptosis, which was detected by levels of phosphatidylserine from the internal to the external membrane and formation of sub-G1, and genotoxicity, which was detected by cytokinesis-blocked micronucleus and single-cell gel electrophoresis assays, were inhibited by rutin in a concentration-dependent manner. Rutin suppressed the BisGMA-induced activation of caspase-3 and -9 rather than caspase-8. Rutin inhibited the activation of the mitochondrial apoptotic pathway, including cytochrome C release and mitochondria disruption, after macrophages were treated with BisGMA. Finally, BisGMA-induced reactive oxygen species (ROS) generation and antioxidant enzyme (AOE) deactivation could be reversed by rutin. Parallel trends were observed in the elevation of AOE activation and inhibition of ROS generation, caspase-3 activity, mitochondrial apoptotic pathway activation, and genotoxicity. These results suggested that rutin suppressed BisGMA-induced cytotoxicity through genotoxicity, the mitochondrial apoptotic pathway, and relatively upstream factors, including reduction of ROS generation and induction of AOE.

E3 ligase STUB1 attenuates stemness and tumorigenicity of oral carcinoma cells via transglutaminase 2 regulation.

BACKGROUND/PURPOSE: Oral cancer is amongst the most prevalent cancers worldwide with rising incidence. Various attempts have been made to elucidate its pathogenesis, and we sought to examine the function of a ubiquitin E3 ligase that was encoded by STUB1. METHODS: The mRNA expression of STUB1 in oral cancer samples and normal counterparts was determined by qRT-PCR. Numerous assays to assess the features of cancer cells, including self-renewal capacity, invasion and migration abilities were conducted following knockdown or overexpression of STUB1. RESULTS: The expression level of STUB1 was reduced in oral cancer, which was associated with a reduced relapse-free survival. Two oral cancer cell lines with low expression of STUB1 (SAS and HSC3) were chosen for the overexpression of STUB1. We showed that ectopic expression of STUB1 led to the downregulation of TGM2, a multifunctional protein that contributed to cancer progression in several cancers. Our results demonstrated that overexpression of STUB1 suppressed the cancer aggressiveness, while restoration of TGM2 reverted the effects. Last, we showed that STUB1 silencing resulted in enhanced cancer features. CONCLUSION: The abnormal downregulation of STUB1 may lessen its suppressive effect on TGM2, which induced the onset or exacerbated the progression of oral cancer. The therapeutic approach to enhance the expression of STUB1 could be a promising direction for cancer therapy.

Influence of PM2.5 Exposure Level on the Association between Alzheimer's Disease and Allergic Rhinitis: A National Population-Based Cohort Study.

Alzheimer's disease (AD) is an irreversible neurodegenerative disease that leads to dementia, health impairment, and high economic cost. Allergic rhinitis (AR) is a chronic inflammatory and allergic disease of the respiratory system that leads to health problems and has major effects on the daily lives of patients and their caregivers. Particulate matter (PM) refers to air pollutants 2.5 µm or less in diameter that are a source of concern because of their role in numerous diseases, including AR and other neurodegenerative diseases. To date, no study has demonstrated how PM2.5 exacerbates AR and results in AD. We conducted a national population-based cohort study by obtaining patient data from the National Health Insurance Research Database of Taiwan for the 2008-2013 period. PM2.5 concentration data were obtained from the ambient air quality monitoring network established by the Environmental Protection Administration of Taiwan. Monthly PM2.5 exposure levels were categorized into quartiles from Q1-Q4. The Cox proportional hazards analysis, after adjusting for age, sex, low income, and urbanization level, revealed that patients with AR had an elevated risk of developing AD (hazard ratio (HR): 2.008). In addition, the cumulative incidence of AD in the AR group was significantly higher than in the comparison group. The PM2.5 levels at Q2-Q4 (crude HR: 1.663-8.315; adjusted HR: 1.812-8.981) were stratified on the basis of the PM2.5 exposure group and revealed that AR patients exposed to PM2.5 are significantly prone to develop AD. In addition, the logistic regression analyses, after adjustment, demonstrated that an increase in the PM2.5 exposure level at Q2-Q4 (adjusted odds ratio (OR): 2.656-5.604) increased the risk of AR in AD patients. In conclusion, an increased PM2.5 exposure level could be correlated with AR, which could in turn cause AD. AR increased the risk of AD, in which exposure to PM2.5 increases the higher probability of AD.