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BACKGROUND: Air pollution is recognized as a modifiable risk factor for dementia, and recent evidence suggests that improving air quality could attenuate cognitive decline and reduce dementia risk. However, studies have yet to explore the effects of improved air quality on brain structures. This study aims to investigate the impact of air pollution reduction on cognitive functions and structural brain differences among cognitively normal older adults. METHODS: Four hundred and thirty-one cognitively normal older adults were from the Epidemiology of Mild Cognitive Impairment study in Taiwan (EMCIT), a community-based cohort of adults aged 60 and older, between year 2017- 2021. Annual concentrations of PM2.5, NO2, O3, and PM10 at participants' residential addresses during the 10 years before enrollment were estimated using ensemble mixed spatial models. The yearly rate of change (slope) in air pollutants was estimated for each participant. Cognitive functions and structural brain images were collected during enrollment. The relationships between the rate of air pollution change and cognitive functions were examined using linear regression models. For air pollutants with significant findings in relation to cognitive function, we further explored the association with brain structure. RESULTS: Overall, all pollutant concentrations, except O3, decreased over the 10-year period. The yearly rates of change (slopes) in PM2.5 and NO2 were correlated with better attention (PM2.5: r = -0.1, p = 0.047; NO2: r = -0.1, p = 0.03) and higher white matter integrity in several brain regions. These regions included anterior thalamic radiation, superior longitudinal fasciculus, inferior longitudinal fasciculus, corticospinal tract, and inferior fronto-occipital fasciculus. CONCLUSIONS: Greater rate of reduction in air pollution was associated with better attention and attention-related white matter integrity. These results provide insight into the mechanism underlying the relationship between air pollution, brain health, and cognitive aging among older adults.
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The study aimed to evaluate the impact of occupational noise on hearing loss among healthcare workers using audiometry. A longitudinal study was conducted with a six-month follow-up period in a hospital with 21 participants, divided into high-noise-exposure (HNE) and low-noise-exposure (LNE) groups. Mean noise levels were higher in the HNE group (70.4 ± 4.5 dBA), and hearing loss was measured using pure-tone audiometry at baseline and follow-up. The HNE group had significantly higher mean threshold levels at frequencies of 0.25 kHz, 0.5 kHz, 4.0 kHz, and an average of 0.5, 1, 2, and 4 kHz (all p-values < 0.05) after the follow-up period. After adjusting for confounding factors, the HNE group had significantly higher hearing loss levels at 0.25 kHz, 0.5 kHz, and average frequencies of 0.5, 1, 2, and 4 kHz compared to the LNE group at the second measurement. Occupational noise levels above 65 dBA over six months were found to cause significant threshold changes at frequencies of 0.25 kHz, 0.5 kHz, and an average of 0.5-4.0 kHz. This study highlights the risk of noise-induced hearing loss among healthcare workers and emphasizes the importance of implementing effective hearing conservation programs in the workplace. Regular monitoring and assessment of noise levels and hearing ability, along with proper use of personal protective equipment, are crucial steps in mitigating the impact of occupational noise exposure on the hearing health of healthcare workers.
Subject(s)
Hearing Loss, Noise-Induced , Noise, Occupational , Occupational Diseases , Occupational Exposure , Humans , Longitudinal Studies , Noise, Occupational/adverse effects , Hearing Loss, Noise-Induced/epidemiology , Personnel, Hospital , HearingABSTRACT
Background: Proton-pump inhibitors (PPIs) are prescribed to treat gastric acid-related diseases, while they may also have potential risks to population health. Recent studies suggested that a potential mechanism explaining the association between PPIs and cardiovascular diseases (CVD) includes the inhibition of the nitrate-nitrite-nitric oxide (NO) pathway. However, previous observational studies showed controversial results of the association. In addition, the inhibition of the NO pathway due to PPIs use may lead to peripheral vascular diseases (PVD); however, none of the studies explore the PPI-PVD association. Therefore, this study aimed to evaluate the association of PPIs with circulatory diseases (CVD, ischemic strokes or IS, and PVD). Methods: We conducted a retrospective hospital-based cohort study from Oct 2010 to Sep 2017 in Songkhla province, Thailand. PPIs and histamine 2-receptor antagonists (H2RAs) prescriptions were collected from electronic pharmacy records, while diagnostic outcomes were retrieved from electronic medical records at Songklanagarind hospital. Patients were followed up with an on-treatment approach. Cox proportional hazard models were applied to measure the association comparing PPIs vs H2RAs after 1:1 propensity-score-matching. Sub-group analysis, multi-bias E-values, and array-based sensitivity analysis for some covariates were used to assess the robustness of associations. Results: A total of 3,928 new PPIs and 3,928 H2RAs users were included in the 1:1 propensity score-matched cohort. As compared with H2RAs, the association of PPIs with CVD, IS, and PVD, the hazard ratios were 1.76 95% CI = [1.40-2.20] for CVD, 3.53 95% CI = [2.21-5.64] for ischemic strokes, and 17.07 95% CI = [13.82-76.25] for PVD. The association between PPIs and each outcome was significant with medication persistent ratio of over 50%. In addition, the association between PPIs and circulatory diseases was robust to unmeasured confounders (i.e., smoking and alcohol). Conclusion: PPIs were associated with circulatory diseases, particularly ischemic strokes in this hospital-based cohort study, whereas, the strength of associations was robust to unmeasured confounders.
Subject(s)
Cardiovascular Diseases , Ischemic Stroke , Peripheral Vascular Diseases , Humans , Proton Pump Inhibitors/adverse effects , Retrospective Studies , Cohort Studies , Cardiovascular Diseases/chemically induced , Electronic Health Records , Thailand/epidemiology , Histamine H2 Antagonists/adverse effects , Peripheral Vascular Diseases/chemically induced , Ischemic Stroke/chemically inducedABSTRACT
BACKGROUND: Ambient particulate matter is classified as a human Class 1 carcinogen, and recent studies found a positive relationship between fine particulate matter (PM2.5) and liver cancer. Nevertheless, little is known about which specific metal constituent contributes to the development of liver cancer. OBJECTIVE: To evaluate the association of long-term exposure to metal constituents in PM2.5 with the risk of liver cancer using a Taiwanese cohort study. METHODS: A total of 13,511 Taiwanese participants were recruited from the REVEAL-HBV in 1991-1992. Participants' long-term exposure to eight metal constituents (Ba, Cu, Mn, Sb, Zn, Pb, Ni, and Cd) in PM2.5 was based on ambient measurement in 2002-2006 followed by a land-use regression model for spatial interpolation. We ascertained newly developed liver cancer (ie, hepatocellular carcinoma [HCC]) through data linkage with the Taiwan Cancer Registry and national health death certification in 1991-2014. A Cox proportional hazards model was utilized to assess the association between exposure to PM2.5 metal component and HCC. RESULTS: We identified 322 newly developed HCC with a median follow-up of 23.1 years. Long-term exposure to PM2.5 Cu was positively associated with a risk of liver cancer. The adjusted hazard ratio (HR) was 1.13 (95% confidence interval [CI], 1.02-1.25; P = 0.023) with one unit increment on Cu normalized by PM2.5 mass concentration in the logarithmic scale. The PM2.5 Cu-HCC association remained statistically significant with adjustment for co-exposures to other metal constituents in PM2.5. CONCLUSION: Our findings suggest PM2.5 containing Cu may attribute to the association of PM2.5 exposure with liver cancer.
Subject(s)
Air Pollutants , Air Pollution , Carcinoma, Hepatocellular , Liver Neoplasms , Humans , Liver Neoplasms/epidemiology , Cohort Studies , Carcinoma, Hepatocellular/epidemiology , Hepatitis B virus , Japan , Particulate Matter/adverse effects , Metals , Environmental Exposure/adverse effectsABSTRACT
BACKGROUND: Exposure to greenness has been shown to be beneficial to health, but few studies have examined the association between residential greenness and prostate cancer (PCa) risk. Our main objectives were to identify the determinants of residential greenness, and to investigate if residential greenness was associated with PCa risk in Singapore. METHODS: The hospital-based case-control study was conducted between April 2007 and May 2009. The Singapore Prostate Cancer Study (SPCS) comprised 240 prostate cancer cases and 268 controls, whose demographics and residential address were collected using questionnaires. Residential greenness was measured by normalized difference vegetation index (NDVI) around the participants' homes using a buffer size of 1 km. Determinants of NDVI were identified using a multivariable linear regression model. Logistic regression models were used to calculate the odds ratios (ORs) and 95% confidence intervals (CIs) of associations between NDVI and PCa risk, adjusting for potential confounders. RESULTS: Having a BMI within the second quartile, as compared to the lowest quartile, was associated with higher levels of NDVI (ß-coefficient = 0.263; 95% CI = 0.040-0.485) after adjusting for covariates. Additionally, being widowed or separated, as compared to being married, was associated with lower levels of NDVI (ß-coefficient = -0.393; 95% CI = -0.723, -0.063). An interquartile range (IQR) increase in NDVI was positively associated with prostate cancer risk OR = 1.45; 95% CI = 1.02-2.07). Stratified analysis by tumour grade and stage showed that higher NDVI was associated with higher risk of low grade PCa. CONCLUSION: Our findings suggested that residential greenness was associated with higher risk of PCa in Singapore. Future studies on the quality and type of green spaces, as well as other factors of residential greenness, in association with PCa risk should be conducted to better understand this relationship.
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It is generally established that PCDD/Fs is harmful to human health and therefore extensive field research is necessary. This study is the first to use a novel geospatial-artificial intelligence (Geo-AI) based ensemble mixed spatial model (EMSM) that integrates multiple machine learning algorithms and geographic predictor variables selected using SHapley Additive exPlanations (SHAP) values to predict spatial-temporal fluctuations in PCDD/Fs concentrations across the entire island of Taiwan. Daily PCDD/F I-TEQ levels from 2006 to 2016 were used for model construction, while external data was used for validating model dependability. We utilized Geo-AI, incorporating kriging, five machine learning, and ensemble methods (combinations of the aforementioned five models) to develop EMSMs. The EMSMs were used to estimate long-term spatiotemporal variations in PCDD/F I-TEQ levels, considering in-situ measurements, meteorological factors, geospatial predictors, social and seasonal influences over a 10-year period. The findings demonstrated that the EMSM was superior to all other models, with an increase in explanatory power reaching 87 %. The results of spatial-temporal resolution show that the temporal fluctuation of PCDD/F concentrations can be a result of weather circumstances, while geographical variance can be the result of urbanization and industrialization. These results provide accurate estimates that support pollution control measures and epidemiological studies.
Subject(s)
Air Pollutants , Benzofurans , Polychlorinated Dibenzodioxins , Humans , Polychlorinated Dibenzodioxins/analysis , Dibenzofurans , Artificial Intelligence , Taiwan , Dibenzofurans, Polychlorinated/analysis , Benzofurans/analysis , Environmental Monitoring/methods , Air Pollutants/analysisABSTRACT
Both greenness and air pollution have widely been linked with asthma. However, the potential mechanism has rarely been investigated. This study aimed to identify the association between residential greenness and air pollution (fine particulate matter [PM2.5]; nitrogen dioxide [NO2]; ozone [O3]) with nasal microbiota among asthmatic children during the recovery phase. The normalized difference vegetation index was used to assess the extent of residential greenness. Spatiotemporal air pollution variation was estimated using an integrated hybrid kriging-LUR with the XG-Boost algorithm. These exposures were measured in 250-m intervals for four incremental buffer ranges. Nasal microbiota was collected from 47 children during the recovery phase. A generalized additive model controlled for various covariates was applied to evaluate the exposure-outcome association. The lag-time effect of greenness and air pollution related to the nasal microbiota also was examined. A significant negative association was observed between short-term exposure to air pollution and nasal bacterial diversity, as a one-unit increment in PM2.5 or O3 significantly decreased the observed species (PM2.5: -0.59, 95%CI -1.13, -0.05 and O3: -0.93, 95%CI -1.54, -0.32) and species richness (PM2.5: -0.64, 95%CI -1.25, -0.02 and O3: -0.68, 95%CI -1.43, -0.07). Considering the lag-time effect, we found a significant positive association between greenness and both the observed species and species richness. In addition, we identified a significant negative association for all pollutants with the observed species richness. These findings add to the evidence base of the links between nasal microbiota and air pollution and greenness. This study establishes a foundation for future studies of how environmental exposure plays a role in nasal microbiota, which in turn may affect the development of asthma.
Subject(s)
Air Pollutants , Air Pollution , Asthma , Humans , Child , Air Pollutants/analysis , Air Pollution/adverse effects , Air Pollution/analysis , Asthma/epidemiology , Particulate Matter/analysis , Environmental Exposure/analysis , Nitrogen Dioxide/analysisABSTRACT
Purpose: Potential adverse outcomes of Proton pump inhibitors (PPIs) have increasingly been reported. The potential risks to PPIs include hypomagnesemia and chronic kidney disease (CKD). Unlike a real-world electronic medical record (RW-EMR) with active-comparator design, claim databases and special population cohort with non-user design, using in previous studies, resulted in a wide range of strength of association with indication bias. This study aimed to measure the total effect of association between PPIs use and CKD incidence using Thai RW-EMR. Patients and Methods: A retrospective hospital-based cohort was applied into this study. Electronic medical records and administrative data of out- and inpatient were retrieved from October 1st, 2010 to September 30th, 2017. On-treatment with grace period as well as propensity score matching was used in data analysis. Cox proportional hazard models were applied to evaluate the PPIs-CKD association. Results: Of all 63,595 participants, a total of 59,477 new PPIs and 4118 Histamine 2-receptor antagonist (H2RA) users were eligible for follow-up. As compared with H2RA, the PPI users were non-elderly and more likely being female. The association of PPIs with CKD was statistically significant (adjusted hazard ratio [HR] = 3.753, 95% CI = 2.385-5.905). The HR were not statistically different by concomitant use PPIs with NSAIDs and by medication possession ratio levels. Conclusion: The association between PPIs and CKD incidence was statistically significant in this hospital-based cohort. However, self-treatment with over-the-counter PPIs, as well as, smoking, drinking alcohol and body mass index could not be fully retrieved, affecting the estimation of treatment effect.
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Objective: Prior studies have shown that greenness can reduce the burden of depressive disorders. However, most were focused on local-scale analyses while limited evaluated globally. We aimed to investigate the association between greenness and the burden of depressive disorders using data from 183 countries worldwide. Methods: We used the normalized difference vegetation index (NDVI) to estimate greenness. Country-level disability-adjusted life year (DALY) loss due to depressive disorders was used to represent depressive disorder burdens. A generalized linear mixed model was applied to assess the relationship between greenness and depressive disorders after controlling for covariates. Stratified analyses were conducted to determine the effects of greenness across several socio-demographic levels. Results: The findings showed a significant negative association between greenness and the health burden of depressive disorders with a coefficient of -0.196 (95% CI: -0.356, -0.035) in the DALY changes per interquartile unit increment of NDVI. The stratified analyses suggested beneficial effects of greenness on depressive disorders across sex, various age groups especially for those aged <49 years, with low-income and/or those living in highly urbanized countries. Conclusions: Our study noted that greenness exposure was significant negative association with the burden of depressive disorders. The findings should be viewed as recommendations for relevant authorities in supporting environmental greenness enhancement to reduce the mental burdens.
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Objective: This study applied an ecological-based analysis aimed to evaluate on a global scale the association between greenness exposure and suicide mortality. Methods: Suicide mortality data provided by the Institute for Health Metrics and Evaluation and the Normalized Difference Vegetation Index (NDVI) were employed. The generalized additive mixed model was applied to evaluate with an adjustment of covariates the association between greenness and suicide mortality. Sensitivity tests and positive-negative controls also were used to examine less overt insights. Subgroup analyses were then conducted to investigate the effects of greenness on suicide mortality among various conditions. Results: The main finding of this study indicates a negative association between greenness exposure and suicide mortality, as greenness significantly decreases the risk of suicide mortality per interquartile unit increment of NDVI (relative risk = 0.69, 95%CI: 0.59-0.81). Further, sensitivity analyses confirmed the robustness of the findings. Subgroup analyses also showed a significant negative association between greenness and suicide mortality for various stratified factors, such as sex, various income levels, urbanization levels, etc. Conclusions: Greenness exposure may contribute to a reduction in suicide mortality. It is recommended that policymakers and communities increase environmental greenness in order to mitigate the global health burden of suicide.
Subject(s)
Suicide Prevention , HumansABSTRACT
Prenatal perfluoroalkyl substance (PFAS) exposure has been linked to adverse birth outcomes, but the underlying mechanism has yet to be elucidated. DNA methylation changes in mesoderm-specific transcript (MEST) imprinted gene may be a mechanism of the prenatal exposure effects of PFASs on fetal growth. The aim was to investigate the prenatal PFASs exposure effects on DNA methylation changes in MEST imprinted gene involved in fetal growth. Among 486 mother-infant pairs from the Taiwan Birth Panel Study, PFASs and DNA methylation levels at 5 CpG sites of MEST promoter region were measured in cord blood. Univariable and multivariable linear regressions were performed to estimate the associations between prenatal PFAS exposure, MEST DNA methylation levels, and child birth outcomes. Mediation analysis was performed to examine the potential pathway of MEST methylation between PFASs and birth outcomes. We found that higher prenatal perfluorooctyl sulfonate (PFOS) exposure was significantly associated with lower methylation levels at 5 CpG sites of MEST promoter region (an adjusted ß range: -1.56, -2.22). Significant negative associations were also found between MEST methylation levels and child birth weight. Furthermore, the associations between PFOS and perfluorooctanoic acid (PFOA) exposure and MEST methylation levels were more profound in girls than in boys. The mediated effect of average MEST methylation level between PFOS exposure and birth weight was 18.3 (95% CI = 2.1, 40.2; p = 0.014). The direct effect of PFOS exposure to birth weight independent to average MEST methylation level was -93.2 (95% CI = -170.5, -17.8; p = 0.018). In conclusion, our results suggest that prenatal PFAS exposure, especially PFOS, is associated with lower methylation levels at MEST promoter region, which not only leverages the role of imprinted gene in ensuring the integrity of fetal growth but also provides a potential mechanism for evaluating the prenatal exposure effect.
Subject(s)
Alkanesulfonic Acids , Environmental Pollutants , Fluorocarbons , Prenatal Exposure Delayed Effects , Alkanesulfonates , Alkanesulfonic Acids/toxicity , Birth Weight , DNA Methylation , Environmental Pollutants/toxicity , Female , Fluorocarbons/toxicity , Humans , Infant , Male , Pregnancy , Prenatal Exposure Delayed Effects/chemically inducedABSTRACT
Exposure to particulate matter with a diameter < 2.5 µm (PM2.5) increases the risk of cardiovascular disease (CVD), which is the leading cause of both morbidity and mortality in Indonesia, accounting for one-third of all deaths. Indonesian authorities started to monitor PM2.5 levels in urban areas in 2015. However, there is still no study examining the association between long-term PM2.5 exposure and CVD in Indonesia. In this study, we combined PM2.5 data and health survey data. Long-term (2000-2007) exposure to PM2.5 was measured based on satellite-derived aerosol optical depth measurements (1 × 1 km2) that could be used to predict ground-level PM2.5 concentrations. Population data on residents of Sumatra Island were obtained from the fourth wave of the Indonesian Family Life Survey (IFLS). A cross-sectional study was performed with 2324 participants who were aged ≥ 40 years old, and a report of doctor-diagnosed CVD determined CVD status. We used logistic regression to analyze the association between PM2.5 and CVD prevalence, adjusting for multiple covariates. Of the sample, 52.1% were women, and 47.9% were men. The sample was divided into those aged 40-59 (adults) and those ≥ 60 (older adults). The CVD prevalence was 4.05% (n = 94), with a mean (standard deviation) PM2.5 concentration of 14.4 (6.4) µg/m3. In adjusted models, a 10-µg/m3 increase in annual average PM2.5 levels was associated with 29% higher odds of having CVD (odds ratio = 1.29; 95% confidence interval: 1.02, 1.47). In this population-based IFLS data, long-term exposure to PM2.5 is associated with a higher prevalence of CVD in Sumatera, Indonesia.
Subject(s)
Air Pollutants , Air Pollution , Cardiovascular Diseases , Adult , Aged , Air Pollutants/analysis , Air Pollution/analysis , Cross-Sectional Studies , Environmental Exposure/analysis , Family Characteristics , Female , Humans , Indonesia/epidemiology , Male , Middle Aged , Particulate Matter/analysisABSTRACT
The proportion of allergic diseases attributable to atopy remains a subject of controversy. This study aimed to estimate the population risk of physician-diagnosed asthma, rhinitis and eczema attributed to atopy among a population sample of Asian school-age children. Asian children aged 5-18 years (n = 1321) in the Prediction of Allergies in Taiwanese CHildren (PATCH) study were tested for serum allergen-specific immunoglobulin E. Physician-diagnosed asthma, rhinitis and eczema were assessed by a modified International Study of Asthma and Allergies in Childhood questionnaire. Atopy was defined as the presence of serum allergen-specific immunoglobulin E. In this population-based study, 50.4% of the subjects with asthma, 46.3% with rhinitis, and 46.7% with eczema were attributable to atopy. The population attributable risk (PAR) of atopy for three allergic diseases was higher in adolescents (asthma, 54.4%; rhinitis, 59.6%; eczema, 49.5%) than younger children aged less than 10 years (asthma, 46.9%; rhinitis, 39.5%; eczema, 41.9%). Among the seven allergen categories, sensitization to mites had the highest PARs for all three allergic diseases (51.3 to 64.1%), followed by sensitization to foods (asthma, 7.1%; rhinitis, 10.4%; eczema 27.7%). In conclusion, approximately half (46.3 to 50.4%) of Asian children in Taiwan with allergic diseases are attributable to atopy.
Subject(s)
Asthma/epidemiology , Eczema/epidemiology , Hypersensitivity, Immediate/complications , Rhinitis/epidemiology , Asthma/etiology , Asthma/pathology , Child , Eczema/etiology , Eczema/pathology , Female , Humans , Hypersensitivity, Immediate/immunology , Immunoglobulin E/immunology , Male , Prevalence , Rhinitis/etiology , Rhinitis/pathology , Risk Factors , Surveys and Questionnaires , Taiwan/epidemiologyABSTRACT
This study aimed to identify the spatial patterns of lower respiratory tract infections (LRIs) and their association with fine particulate matter (PM2.5). The disability-adjusted life year (DALY) database was used to represent the burden each country experiences as a result of LRIs. PM2.5 data obtained from the Atmosphere Composition Analysis Group was assessed as the source for main exposure. Global Moran's I and Getis-Ord Gi* were applied to identify the spatial patterns and for hotspots analysis of LRIs. A generalized linear mixed model was coupled with a sensitivity test after controlling for covariates to estimate the association between LRIs and PM2.5. Subgroup analyses were performed to determine whether LRIs and PM2.5 are correlated for various ages and geographic regions. A significant spatial auto-correlated pattern was identified for global LRIs with Moran's Index 0.79, and the hotspots of LRIs were clustered in 35 African and 4 Eastern Mediterranean countries. A consistent significant positive association between LRIs and PM2.5 with a coefficient of 0.21 (95% CI 0.06-0.36) was identified. Furthermore, subgroup analysis revealed a significant effect of PM2.5 on LRI for children (0-14 years) and the elderly (≥ 70 years), and this effect was confirmed to be significant in all regions except for those comprised of Eastern Mediterranean countries.
Subject(s)
Air Pollution/adverse effects , Global Health , Particulate Matter/adverse effects , Respiratory Tract Infections/epidemiology , Adolescent , Adult , Aged , Child , Child, Preschool , Female , Humans , Infant , Infant, Newborn , Male , Middle Aged , Risk FactorsSubject(s)
Air Pollutants , Air Pollution , Eczema , Prenatal Exposure Delayed Effects , Air Pollutants/analysis , Air Pollution/adverse effects , Air Pollution/analysis , Child , Eczema/chemically induced , Eczema/epidemiology , Environmental Exposure/adverse effects , Female , Humans , Maternal Exposure/adverse effects , Particulate Matter/adverse effects , Pregnancy , Prenatal Exposure Delayed Effects/epidemiologyABSTRACT
BACKGROUND: To date, there is no comprehensive study examining how asthma diagnosed in childhood or adolescence is associated with diagnoses of subsequent non-communicable diseases (NCDs) during adulthood. Our study aimed to examine the associations between pediatric asthma and several adult NCDs, with temporality and long interval times between asthma and NCD diagnoses. METHODS: We used RAND Indonesian Family Life Survey Fifth Wave (IFLS5) fielded in 2014-2015, to study whether being diagnosed with pediatric asthma at 0-19 years of age was associated with increased risks of hypertension, diabetes, rheumatoid arthritis, stomach diseases, kidney diseases, and heart diseases or stroke diagnosed in adulthood. We used the weighted Poisson regression adjusting for age, sex, urbanicity, and insurance status to estimate risk ratios. Subgroup analyses were performed by sex and age of asthma and other NCD diagnoses. RESULTS: Pediatric asthma significantly increased risks of hypertension, diabetes, and stomach diseases diagnosed at 20 years of age or above. Males with pediatric asthma diagnosed at 0-10 years of age had significantly higher risk of hypertension, while females with pediatric asthma diagnosed at 0-10 years of age had significantly higher risks of diabetes and stomach diseases. Females with pediatric asthma diagnosed at 11-19 years of age had significantly higher risks of diabetes, arthritis, stomach diseases, and kidney diseases. We also found varying associations by age of NCD diagnosis. CONCLUSION: Our results suggest pediatric asthma is associated with increased risks of several adult NCDs, and these associations may vary by sex and age of asthma and other NCD diagnoses.
Subject(s)
Asthma , Diabetes Mellitus , Hypertension , Noncommunicable Diseases , Adolescent , Adult , Asthma/epidemiology , Child , Female , Humans , Infant, Newborn , Male , Noncommunicable Diseases/epidemiology , Risk FactorsABSTRACT
BACKGROUND: Exposure to traffic-related pollution is positively associated with cardiovascular diseases (CVD), but little is known about how different sources of traffic pollution (eg, gasoline-powered cars, diesel-engine vehicles) contribute to CVD. Therefore, we evaluated the association between exposure to different types of engine exhaust and CVD mortality. METHODS: We recruited 12,098 participants from REVEAL-HBV cohort in Taiwan. The CVD mortality in 2000-2014 was ascertained by the Taiwan Death Certificates. Traffic pollution sources (2005-2013) were based on information provided by the Directorate General of Highway in 2005. Exposure to PM2.5 was based on a land-use regression model. We applied Cox proportional hazard models to assess the association of traffic vehicle exposure and CVD mortality. A causal mediation analysis was applied to evaluate the mediation effect of PM2.5 on the relationship between traffic and CVD mortality. RESULTS: A total of 382 CVD mortalities were identified from 2000 to 2014. We found participants exposed to higher volumes of small car and truck exhausts had an increased CVD mortality. The adjusted hazard ratio (HR) was 1.10 for small cars (95% confidence interval [CI], 0.94-1.27; P-value = 0.23) and 1.24 for truck (95% CI, 1.03-1.51; P-value = 0.03) per one unit increment of the logarithm scale. The findings were still robust with further adjustment for different types of vehicles. A causal mediation analysis revealed PM2.5 had an over 60% mediation effect on traffic-CVD association. CONCLUSIONS: Exposure to exhaust from trucks or gasoline-powered cars is positively associated with CVD mortality, and air pollution may play a role in this association.
Subject(s)
Automobile Driving/statistics & numerical data , Cardiovascular Diseases/mortality , Environmental Exposure/adverse effects , Traffic-Related Pollution/adverse effects , Vehicle Emissions/poisoning , Adult , Aged , Environmental Exposure/statistics & numerical data , Female , Humans , Male , Middle Aged , Proportional Hazards Models , Prospective Studies , Taiwan/epidemiology , Traffic-Related Pollution/statistics & numerical data , Vehicle Emissions/analysisABSTRACT
SCOPE: Coffee and tea are among the most popular beverages in the world. However, the association between habitual coffee, green tea, and black tea consumption with metabolomics profiles in Asian populations remain largely unknown. METHODS AND RESULTS: 158 metabolites (14 amino acids, 45 acylcarnitines, and 99 sphingolipids) in the blood plasma of participants are measured from the population-based Singapore Prospective Study Program cohort using mass spectrometry (MS). Linear regression models are used to obtain the estimates for the association between coffee and tea consumption with metabolite levels, adjusted for potential confounders and false discovery rate (FDR). Coffee consumption is significantly associated with higher levels of 63 sphingolipids (29 sphingomyelins, 32 ceramides, a sphingosine-1-phosphate, and a sphingosine) and lower levels of 13 acylcarnitines and alanine. Black tea consumption is significantly associated with higher levels of eight sphingolipids, and lower levels of an amino acid, whereas green tea is significantly inversely associated with four metabolites (C8:1-OH acylcarnitine, ganglioside GM3 d18:1/16:0, sphingomyelins d18:2/18:0 and d18:1/14:0). CONCLUSIONS: Coffee, black tea, and green tea consumption are associated with plasma levels of certain classes of sphingolipids and acylcarnitines in an Asian population, particularly sphingomyelins, which may mediate the health benefits of these beverages.
ABSTRACT
Exposure to surrounding greenness is associated with reduced mortality in Caucasian populations. Little is known however about the relationship between green vegetation and the risk of death in Asian populations. Therefore, we opted to evaluate the association of greenness with mortality in Taiwan. Death information was retrieved from the Taiwan Death Certificate database between 2006 to 2014 (3287 days). Exposure to green vegetation was based on the normalized difference vegetation index (NDVI) collected by the Moderate Resolution Imagine Spectroradiometer (MODIS). A generalized additive mixed model was utilized to assess the association between NDVI exposure and mortality. A total of 1,173,773 deaths were identified from 2006 to 2014. We found one unit increment on NDVI was associated with a reduced mortality due to all-cause (risk ratio [RR] = 0.901; 95% confidence interval = 0.862-0.941), cardiovascular diseases (RR = 0.892; 95% CI = 0.817-0.975), respiratory diseases (RR = 0.721; 95% CI = 0.632-0.824), and lung cancer (RR = 0.871; 95% CI = 0.735-1.032). Using the green land cover as the alternative green index showed the protective relationship on all-cause mortality. Exposure to surrounding greenness was negatively associated with mortality in Taiwan. Further research is needed to uncover the underlying mechanism.
Subject(s)
Air Pollution/adverse effects , Cardiovascular Diseases/mortality , Environment , Particulate Matter/adverse effects , Residence Characteristics/statistics & numerical data , Adolescent , Adult , Cardiovascular Diseases/chemically induced , Child , Child, Preschool , Female , Humans , Infant , Infant, Newborn , Male , Middle Aged , Mortality , Rural Population , Taiwan/epidemiology , Urban Population , Young AdultABSTRACT
Metabolic syndrome is becoming more common worldwide. Studies suggest environmental pollution, including traffic noise, might be linked with metabolic syndrome. This study sought to evaluate how noise exposure is linked to the development of metabolic syndrome and its components in Taiwan. Using data from a cohort of 42,509 participants and Cox proportional hazards regression models, the effects of noise exposure on metabolic syndrome and its components were quantified. After adjustment for covariates (age, gender, body mass index, and physical activity), the hazard ratio for metabolic syndrome was 1.13 (95% CI: 1.04-1.22) for medium noise exposure and 1.24 (95% CI: 1.13-1.36) for high noise exposure. Noise exposure was also positively associated with all of metabolic syndrome's components. This finding suggests noise exposure might contribute to metabolic syndrome and its components. Policies aiming to reduce noise pollution might reduce the risks of metabolic syndrome and its components.