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Objective: To examine the effects of fish oil supplements on the clinical course of cardiovascular disease, from a healthy state to atrial fibrillation, major adverse cardiovascular events, and subsequently death. Design: Prospective cohort study. Setting: UK Biobank study, 1 January 2006 to 31 December 2010, with follow-up to 31 March 2021 (median follow-up 11.9 years). Participants: 415 737 participants, aged 40-69 years, enrolled in the UK Biobank study. Main outcome measures: Incident cases of atrial fibrillation, major adverse cardiovascular events, and death, identified by linkage to hospital inpatient records and death registries. Role of fish oil supplements in different progressive stages of cardiovascular diseases, from healthy status (primary stage), to atrial fibrillation (secondary stage), major adverse cardiovascular events (tertiary stage), and death (end stage). Results: Among 415 737 participants free of cardiovascular diseases, 18 367 patients with incident atrial fibrillation, 22 636 with major adverse cardiovascular events, and 22 140 deaths during follow-up were identified. Regular use of fish oil supplements had different roles in the transitions from healthy status to atrial fibrillation, to major adverse cardiovascular events, and then to death. For people without cardiovascular disease, hazard ratios were 1.13 (95% confidence interval 1.10 to 1.17) for the transition from healthy status to atrial fibrillation and 1.05 (1.00 to 1.11) from healthy status to stroke. For participants with a diagnosis of a known cardiovascular disease, regular use of fish oil supplements was beneficial for transitions from atrial fibrillation to major adverse cardiovascular events (hazard ratio 0.92, 0.87 to 0.98), atrial fibrillation to myocardial infarction (0.85, 0.76 to 0.96), and heart failure to death (0.91, 0.84 to 0.99). Conclusions: Regular use of fish oil supplements might be a risk factor for atrial fibrillation and stroke among the general population but could be beneficial for progression of cardiovascular disease from atrial fibrillation to major adverse cardiovascular events, and from atrial fibrillation to death. Further studies are needed to determine the precise mechanisms for the development and prognosis of cardiovascular disease events with regular use of fish oil supplements.
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BACKGROUND: The association of pre-diabetes and type 2 diabetes (T2D) with incident lung cancer is uncertain, and the incident risk across the glycemic spectrum is unclear. We aimed to explore the associations of glycosylated hemoglobin (HbA1c), pre-diabetes, and T2D with incident lung cancer in a large prospective cohort. METHODS: Leveraging a total of 210,779 cancer-free adults recruited in the UK Biobank between 2006 and 2010. We performed multivariable Cox proportional hazards models and restricted cubic spline methods to estimate hazard ratios (HRs) and 95% confidence intervals (95% CIs) for the associations of HbA1c, pre-diabetes, and T2D with incident lung cancer. RESULTS: During a median follow-up of 11.06 years, 1738 incident lung cancer cases were ascertained. The incidence of lung cancer was 20% higher among people with diabetes (HR: 1.20, 95% CI: 1.02 to 1.42) and 38% higher among people with pre-diabetes (HR: 1.38, 95% CI: 1.15 to 1.65). After dividing people with diabetes by whether taking antidiabetic medications, the incidence was 28% higher among people with diabetes without medications (HR: 1.28, 95% CI: 1.02 to 1.61) and 15% higher among people with diabetes with medications (HR: 1.15, 95% CI: 0.93 to 1.41). The increased risk of incident lung cancer for each standard deviation (6.45 mmol/mol) increase in HbA1c was more pronounced across HbA1c values of 32-42 mmol/mol (HR: 1.37, 95% CI: 1.18 to 1.59). The risk was more pronounced among participants <60 years. CONCLUSIONS: Pre-diabetes and T2D are associated with an increased incidence of lung cancer. The increased risk of incident lung cancer is more pronounced across HbA1c values of 32-42 mmol/mol, which are currently considered normal values.
Subject(s)
Diabetes Mellitus, Type 2 , Lung Neoplasms , Prediabetic State , Adult , Humans , Diabetes Mellitus, Type 2/complications , Diabetes Mellitus, Type 2/epidemiology , Prediabetic State/epidemiology , Glycated Hemoglobin , Prospective Studies , Lung Neoplasms/epidemiology , Lung Neoplasms/etiology , Risk Factors , IncidenceABSTRACT
BACKGROUND: Although the indoor environment has been proposed to be associated with childhood sleep health, to our knowledge no study has investigated the association between home renovation and childhood sleep problems. METHODS: The study included 186,470 children aged 6-18 years from the National Chinese Children Health Study (2012-2018). We measured childhood sleeping problems via the Chinese version of the Sleep Disturbance Scale for Children (C-SDSC). Information on home renovation exposure within the recent 2 years was collected via parent report. We estimated associations between home renovation and various sleeping problems, defined using both continuous and categorized (binary) C-SDSC t-scores, using generalized mixed models. We fitted models with city as a random effect variable, and other covariates as fixed effects. RESULTS: Out of the overall participants, 89,732 (48%) were exposed to recent home renovations. Compared to the unexposed group, children exposed to home renovations had higher odds of total sleep disorder (odd ratios [OR] = 1.3; 95% confidence interval [CI] = 1.2, 1.4). Associations varied when we considered different types of home renovation materials. Children exposed to multiple types of home renovation had higher odds of sleeping problems. We observed similar findings when considering continuous C-SDSC t-scores. Additionally, sex and age of children modified the associations of home renovation exposure with some of the sleeping problem subtypes. CONCLUSIONS: We found that home renovation was associated with higher odds of having sleeping problems and that they varied when considering the type of renovation, cumulative exposure, sex, and age differences.
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Seizures , Sleep Wake Disorders , Child , Humans , Surveys and Questionnaires , Cities , China/epidemiology , Sleep Wake Disorders/epidemiologyABSTRACT
OBJECTIVES: We aimed to investigate the associations between air pollutants and the risk of admission and multiple readmission events for cardiovascular disease (CVD). METHODS: A total of 285 009 participants free of CVD at baseline from the UK Biobank were included in this analysis. Four major cardiovascular admission events were identified during the follow-up: chronic ischaemic heart disease (CIHD), cerebrovascular disease, atrial fibrillation and heart failure. We used Prentice, Williams and Peterson-Total Time model to examine the association between ambient air pollution and first admission, as well as multiple readmissions for these CVDs. RESULTS: During a median follow-up of 12 years, 17 176 (6.03%) participants were hospitalised with CVDs, and 6203 (36.11%) patients with CVD had subsequent readmission events for CVDs. We observed significant associations between air pollution and both first admission and readmission for CVDs, with generally stronger associations on readmission for cardiovascular events. For example, the adjusted HRs for the first admission and subsequent readmission for cerebrovascular disease were 1.130 (95% CI 1.070 to 1.194) and 1.270 (95% CI 1.137 to 1.418) for each IQR increase of particulate matter with a diameter ≤2.5 µm. The corresponding HRs for CIHD were 1.060 (95% CI 1.008 to 1.114) and 1.120 (95% CI 1.070 to 1.171). Sex stratified analyses showed that the associations were generally more pronounced among females than males. CONCLUSION: This study provides evidence that ambient air pollutants might play an important role in both first admission and readmission for cardiovascular events. In addition, patients with pre-existing CVDs may be more vulnerable to air pollution compared with healthy population.
Subject(s)
Air Pollutants , Air Pollution , Cardiovascular Diseases , Cerebrovascular Disorders , Myocardial Ischemia , Male , Female , Humans , Cardiovascular Diseases/epidemiology , Cardiovascular Diseases/therapy , Cardiovascular Diseases/chemically induced , Patient Readmission , Environmental Exposure/adverse effects , Air Pollution/adverse effects , Air Pollutants/adverse effects , Particulate Matter/adverse effects , Cerebrovascular Disorders/epidemiology , Cerebrovascular Disorders/therapyABSTRACT
Background: Cardiovascular disease (CVD) remains a paramount contemporary health challenge. This study examined age-specific effects of 14 risk factors on CVD and mortality in different age groups. Methods: We analyzed data from 226,759 CVD-free participants aged 40 years and older in the UK Biobank during the period from baseline time (2006-2010) to September 30, 2021. The primary CVD outcome was a composite of incident coronary artery disease, heart failure, and stroke. We calculated age-specific hazard ratios (HRs) and population-attributable fractions (PAF) for CVD and mortality associated with 14 potentially modifiable risk factors. Findings: During 12.17-year follow-up, 23,838 incident CVD cases and 11,949 deaths occurred. Age-specific disparities were observed in the risk factors contributing to CVD, and the overall PAF declined with age (PAF of 56.53% in middle-age; 49.78% in quinquagenarian; 42.45% in the elderly). Metabolic factors had the highest PAF in each age group, with hypertension (14.04% of the PAF) and abdominal obesity (9.58% of the PAF) being prominent. Behavioral factors had the highest PAF in the middle-aged group (10.68% of the PAF), and smoking was the leading behavioral factor in all age groups. In socioeconomic and psychosocial risk clusters, low income contributed most among middle-aged (3.74% of the PAF) and elderly groups (3.66% of the PAF), while less education accounted more PAF for quinquagenarian group (4.46% of the PAF). Similar age-specific patterns were observed for cardiovascular subtypes and mortality. Interpretation: A large fraction of CVD cases and deaths were associated with modifiable risk factors in all age groups. Targeted efforts should focus on the most impactful risk factors, as well as age-specific modifiable risk factors. These findings may inform the development of more precise medical strategies to prevent and manage CVD and related mortality. Funding: The work was supported by the Bill & Melinda Gates Foundation (grant number: INV-016826 to Hualiang Lin) and the National Natural Science Foundation of China (grant number: 82373534 to Hualiang Lin).
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BACKGROUND: Estrogens play a critical role in parturition, and poly- and perfluoroalkyl substances (PFAS), which have estrogenic effects, have been associated with preterm birth. However, the impact of estrogens on the association between PFAS and preterm birth is unknown. OBJECTIVE: The objective of this study is to investigate if estrogens modified the association between PFAS and preterm birth, using a nested case-control study design. METHODS: A total of 371 preterm births and 508 controls were selected from a birth cohort study in China between 2016 and 2018. Perfluorobutanoic acid (PFBA), perfluorohexanesulfonic acid (PFHxS) and its branched isomer, perfluorooctanoic acid (PFOA), perfluorooctanesulfonic acid (PFOS) and its branched isomer, and perfluorononanoic acid (PFNA) were quantified in maternal serum (mean gestational age of 32 wk). Estradiol and estriol were quantified in cord serum. Preterm birth was defined as live delivery at <37 gestational weeks. Causal mediation analysis was used to estimate the mediation and interaction effects of estrogen on the association between PFAS and preterm birth. Latent profile analysis was used to identify important estrogen profiles. Multiple linear regression was used to estimate associations between PFAS and preterm birth and interactions between PFAS and estrogens on preterm birth. RESULTS: Overall, higher odds ratios (ORs) of preterm birth were associated with each 1 ln-unit PFAS increase: PFBA [1.20, 95% confidence interval (CI): 1.14, 1.26], PFNA (1.30, 95% CI: 1.21, 1.39), PFOA (1.98, 95% CI: 1.54, 2.55), and PFOS (1.91, 95% CI: 1.76, 2.07) and its branched isomer (1.91, 95% CI: 1.90, 1.92). We detected statistically significant interactions between cord estradiol and PFAS on preterm birth, while no mediation effects of cord estrogen were observed. The ORs of PFOS (4.29, 95% CI: 1.31, 8.25), its branched isomer (6.71, 95% CI: 1.06, 11.91), and preterm birth were greater for participants with high cord estrogen levels than for participants with low cord estrogen levels. DISCUSSION: Our findings suggest that estrogen modified the association between maternal PFAS exposure and preterm birth. Further studies on maternal PFAS exposure and preterm birth, taking interaction effects of cord estrogens into account, are warranted. https://doi.org/10.1289/EHP11377.
Subject(s)
Fluorocarbons , Premature Birth , Prenatal Exposure Delayed Effects , Infant, Newborn , Female , Pregnancy , Humans , Premature Birth/epidemiology , Case-Control Studies , Cohort Studies , Prenatal Exposure Delayed Effects/epidemiology , Estrogens , EstradiolABSTRACT
A new lithophytic species, Paraboeazunyiensis T.Deng, F.Wen & R.B.Zhang (Gesneriaceae), inhabiting Karst rocks in northern Guizhou, China, is introduced and depicted in this study. It bears a resemblance to P.crassifolia (Hemsl.) B.L. Burtt, yet is distinguishable by its shorter filaments and staminodes, triangular ovate calyx segments, and ovaries surpassing the styles in length. Moreover, the phylogenetic tree constructed from nuclear DNA (ITS) and plastid DNA (trnL-F) data firmly support the differentiation of this novel species from P.crassifolia.
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Background The purpose of this study was to explore the association of sleep patterns with the development of first cardiovascular diseases (FCVD), progression to cardiovascular multimorbidity (CVM), and subsequently to mortality. Methods and Results This prospective study included 381 179 participants without coronary heart disease, stroke, atrial fibrillation, or heart failure at baseline, and they were followed up until March 31, 2021. We generated sleep patterns by summing the scores for 5 sleep behaviors, whereby <7 or >8 hours/d of sleep, evening chronotype, frequent insomnia, snoring, and daytime dozing were defined as high-risk groups. We used a multistate model to estimate the impacts of sleep patterns on the dynamic progression of cardiovascular diseases. Over a median follow-up of 12.1 years, 41 910 participants developed FCVD, 7302 further developed CVM, and 20 707 died. We found that adverse sleep patterns were significantly associated with the transition from health to FCVD, from FCVD to CVM, and from health to death, with hazard ratio associated with 1-factor increase in sleep scores being 1.08 (95% CI, 1.07-1.09), 1.04 (95% CI, 1.02-1.06), and 1.04 (95% CI, 1.02-1.05), respectively. When further dividing FCVD into coronary heart disease, stroke, atrial fibrillation, and heart failure, adverse sleep patterns showed a significant and persistent effect on the transition from health to each cardiovascular disease, and from heart failure or atrial fibrillation to CVM. Conclusions Our study provides evidence that adverse sleep patterns might increase the risk for the progression from health to cardiovascular diseases and further to CVM. Our findings suggest that improving sleep behaviors might be helpful for the primary and secondary prevention of cardiovascular diseases.
Subject(s)
Atrial Fibrillation , Cardiovascular Diseases , Heart Failure , Stroke , Humans , Cardiovascular Diseases/epidemiology , Prospective Studies , Multimorbidity , Heart Failure/epidemiology , Stroke/epidemiology , Sleep , Risk FactorsABSTRACT
BACKGROUND: The association between air pollution and mental disorders has been widely documented in the general population. However, the evidence among susceptible populations, such as individuals with prediabetes or diabetes, is still insufficient. METHODS: We analyzed data from 48,515 participants with prediabetes and 24,393 participants with diabetes from the UK Biobank. Annual pollution data were collected for fine particulate matter (PM2.5), inhalable particulate matter (PM10), nitrogen dioxide (NO2), and nitrogen dioxides (NOx) during 2006-2021. The exposure to air pollution and temperature for each participant were estimated by the bilinear interpolation approach and time-weighted method based on their geocoded home addresses and time spent at each address. We employed the generalized propensity score model based on the generalized estimating equation and the time-varying covariates Cox model to assess the effects of air pollution. RESULTS: We observed causal links between air pollutants and mental disorders among both prediabetic and diabetic participants, with stronger effects among those with diabetes than prediabetes. The hazard ratios were 1.18 (1.12, 1.24), 1.15 (1.10, 1.20), 1.18 (1.13, 1.23), and 1.15 (1.11, 1.19) in patients with prediabetes, and 1.21 (1.13, 1.29), 1.17 (1.11, 1.24), 1.19 (1.13, 1.25), and 1.17 (1.12, 1.23) in patients with diabetes per interquartile range elevation in PM2.5, PM10, NO2, and NOx. Furthermore, the effects were more pronounced among people who were older, alcohol drinkers, and living in urban areas. CONCLUSIONS: Our study indicates the potential causal links between long-term exposure to air pollution and incident mental disorders among those with prediabetes and diabetes. Reducing air pollution levels would significantly benefit this vulnerable population by reducing the incidence of mental disorders.
Subject(s)
Air Pollutants , Air Pollution , Diabetes Mellitus , Mental Disorders , Prediabetic State , Humans , Prediabetic State/epidemiology , Nitrogen Dioxide/analysis , Prospective Studies , Environmental Exposure/analysis , Air Pollution/analysis , Air Pollutants/adverse effects , Air Pollutants/analysis , Particulate Matter/adverse effects , Particulate Matter/analysis , Diabetes Mellitus/epidemiology , Mental Disorders/epidemiologyABSTRACT
This study was envisaged to identify a strain of bacteria isolated from the gill of mandarin fish. Identification and characterization of the bacterial strain were performed using morphological characteristics, growth temperature, physiological and biochemical tests, antibiotic sensitivity tests, artificial infection tests, and 16S rRNA gene sequencing homology analysis. The results showed that the bacterium was Gram-negative, with flagella at the end and the side. The bacterium exhibited a light brownish-gray colony on the Luria-Bertani culture and white colony on the blood agar plate without hemolytic ring. Normal growth was achieved at 42°C, and growth could be delayed in 7% NaCl broth medium. By homology comparison and analysis, the phylogenetic tree was constructed using MEGA7.0, and the bacterium was preliminarily identified as Achromobacter. The antibiotic sensitivity test showed that the strain was sensitive to piperacillin, carbenicillin, cefoperazone, cefazolin, ofloxacin, gentamicin, kanamycin, amikacin, neomycin, erythromycin, minocycline, doxycycline, polymyxin B, tetracycline, chloramphenicol, and other drugs. However, it was resistant to penicillin, ampicillin, oxacillin, ceftriaxone, cefradine, cefalexin, cefuroxime sodium, ciprofloxacin, norfloxacin, vancomycin, compound sulfamethoxazole, clindamycin, medimycin, and furazolidone.
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BACKGROUND: Understanding the effects of risk factor burden and genetic predisposition on the long-term risk of atrial fibrillation (AF) is important to improve public health initiatives. However, the 10-year risk of AF considering risk factor burden and genetic predisposition is unknown. METHODS: A total of 348,904 genetically unrelated participants without AF at baseline from the UK were categorized into three groups: index ages 45 years (n = 84,206), 55 years (n=117,520), and 65 years (n=147,178). Optimal, borderline, or elevated risk factor burden was determined by body mass index, blood pressure, diabetes mellitus, alcohol consumption, smoking status, and history of myocardial infarction or heart failure. Genetic predisposition was estimated using the polygenic risk score (PRS), constructed using 165 predefined genetic risk variants. The combined effects of risk factor burden and PRS on the risk of incident AF in 10 years were estimated for each index age. Fine and Gray models were developed to predict the 10-year risk of AF. RESULTS: The overall 10-year risk of AF was 0.67% (95% CI: 0.61-0.73%) for index age 45 years, 2.05% (95% CI: 1.96-2.13%) for index age 55 years, and 6.34% (95% CI: 6.21-6.46%) for index age 65 years, respectively. An optimal risk factor burden was associated with later AF onset regardless of genetic predisposition and sex (P < 0.001). Significant synergistic interactions were observed for risk factor burden with PRS at each index age (P < 0.05). Participants with an elevated risk factor burden and high PRS had the highest 10-year risk of AF in reference to those who had both an optimal risk factor burden and a low PRS. At younger ages, optimal risk burden and high PRS might also lead to later onset of AF, compared to the joint effect of elevated risk burden and low/intermediate PRS. CONCLUSIONS: Risk factor burden together with a genetic predisposition is associated with the 10-year risk of AF. Our results may be helpful in selecting high-risk individuals for primary prevention of AF and facilitating subsequent health interventions.
Subject(s)
Atrial Fibrillation , Humans , Middle Aged , Aged , Atrial Fibrillation/epidemiology , Atrial Fibrillation/genetics , Prospective Studies , Genetic Predisposition to Disease , Risk Factors , Alcohol DrinkingABSTRACT
BACKGROUND: The relationship between air pollution and stroke has been extensively studied, however, the evidence regarding the association between air pollution and hospitalization due to stroke and its subtypes in coastal areas of China is limited. OBJECTIVE: To estimate the associations between air pollution and hospitalizations of stroke and its subtypes in the Beibu Gulf Region of China. METHODS: We conducted a time-stratified case-crossover study in 15 cities in Beibu Gulf Region in China from 2013 to 2016. Exposures to PM1, PM2.5, PM10, SO2, NO2, O3, and CO on the case and control days were assessed at residential addresses using bilinear interpolation. Conditional logistic regressions were constructed to estimate city-specific associations adjusting for meteorological factors and public holidays. Meta-analysis was further conducted to pool all city-level estimates. RESULTS: There were 271,394 case days and 922,305 control days. The odds ratios (ORs) for stroke hospitalizations associated with each interquartile range (IQR) increase in 2-day averages of SO2 (IQR: 10.8 µg/m3), NO2 (IQR: 11.2 µg/m3), and PM10 (IQR: 37 µg/m3) were 1.047 (95 % CI [confidence interval]: 1.015-1.080), 1.040 (95 % CI: 1.027-1.053), and 1.018 (95 % CI: 1.004-1.033), respectively. The associations with hospitalizations of ischemic stroke were significant for all seven pollutants, while the association with hemorrhagic stroke was significant only for CO. The associations of SO2, NO2, and O3 with stroke hospitalization were significantly stronger in the cool season. CONCLUSIONS: Short-term increase in SO2, NO2, and PM10 might be important triggers of stroke hospitalization. All seven air pollutants were associated with ischemic stroke hospitalization, while only CO was associated with hemorrhagic stroke hospitalization. These results should be considered in public health policy.
Subject(s)
Air Pollutants , Air Pollution , Hemorrhagic Stroke , Ischemic Stroke , Stroke , Humans , Cross-Over Studies , Nitrogen Dioxide/analysis , Particulate Matter/adverse effects , Particulate Matter/analysis , Air Pollution/adverse effects , Air Pollution/analysis , Air Pollutants/adverse effects , Air Pollutants/analysis , Stroke/epidemiology , Hospitalization , China/epidemiologyABSTRACT
BACKGROUND: No prior study has examined the effects of air pollution on the progression from healthy to chronic lung disease, subsequent chronic lung multimorbidity and further to death. METHODS: We used data from the UK Biobank of 265 506 adults free of chronic lung disease at recruitment. Chronic lung multimorbidity was defined as the coexistence of at least two chronic lung diseases, including asthma, chronic obstructive pulmonary disease and lung cancer. The concentrations of air pollutants were estimated using land-use regression models. Multistate models were applied to assess the effect of air pollution on the progression of chronic lung multimorbidity. RESULTS: During a median follow-up of 11.9 years, 13 863 participants developed at least one chronic lung disease, 1055 developed chronic lung multimorbidity and 12 772 died. We observed differential associations of air pollution with different trajectories of chronic lung multimorbidity. Fine particulate matter showed the strongest association with all five transitions, with HRs (95% CI) per 5 µg/m3 increase of 1.31 (1.22 to 1.42) and 1.27 (1.01 to 1.57) for transitions from healthy to incident chronic lung disease and from incident chronic lung disease to chronic lung multimorbidity, and 1.32 (1.21 to 1.45), 1.24 (1.01 to 1.53) and 1.91 (1.14 to 3.20) for mortality risk from healthy, incident chronic lung disease and chronic lung multimorbidity, respectively. CONCLUSION: Our study provides the first evidence that ambient air pollution could affect the progression from free of chronic lung disease to incident chronic lung disease, chronic lung multimorbidity and death.
Subject(s)
Air Pollutants , Air Pollution , Pulmonary Disease, Chronic Obstructive , Adult , Humans , Cohort Studies , Incidence , Environmental Exposure/adverse effects , Environmental Exposure/analysis , Air Pollution/adverse effects , Air Pollution/analysis , Air Pollutants/adverse effects , Air Pollutants/analysis , Particulate Matter/adverse effects , Particulate Matter/analysis , Pulmonary Disease, Chronic Obstructive/epidemiology , Pulmonary Disease, Chronic Obstructive/etiologyABSTRACT
Objectives The relationship between prenatal physical activity (PA) and adverse birth outcomes is still inconclusive. We aimed to investigate the association between PA during pregnancy and adverse birth outcomes by using data from the Guangxi Zhuang birth cohort (GZBC) in China.Study Design A total of 11,292 mother-infant pairs were included from GZBC in China. The information on PA status, intensity, adequacy, and volume and birth outcomes were collected. Multivariable linear and logistic regression models were applied to analyze the effects of PA during pregnancy on birth weight z-scores (BW z-scores) and gestational age and risk of small-for-gestational age (SGA) and preterm birth (PTB), respectively. Cubic spline analysis was conducted to detect a nonlinear dose-response of total weekly activity metabolic equivalents (MET) and birth outcomes.Results Compared to no regular PA during pregnancy, moderate and high-intensity PA (MVPA) was associated with increase BW z-scores (ß = 0.08, 95%CI: 0.002, 0.15, p = .044) and associated with a marginal significant decrease in risk of PTB (OR = 0.73, 95%CI: 0.51, 1.05, p = .093). However, PA had no relationship with gestational age and risk of SGA, and Nonlinear relationships were not observed between total weekly activity MET and risk of SGA and PTB.Conclusion These finding shows that PA during pregnancy may increase the BW z-score and reduce risk of PTB, supporting the guidelines that pregnant women should be encouraged to engage in appropriate physical activity during pregnancy in China.
Subject(s)
Premature Birth , Pregnancy , Infant, Newborn , Humans , Female , Premature Birth/epidemiology , Prospective Studies , China/epidemiology , Infant, Small for Gestational Age , Birth Weight , Parturition , Fetal Growth Retardation , Exercise , Pregnancy Outcome/epidemiologyABSTRACT
BACKGROUND: The associations between air pollution exposure and morbidity and mortality of cardiovascular diseases (CVDs) have been widely reported; however, evidence on such associations across different dynamic disease trajectories remain unknown. OBJECTIVE: We examined whether ambient air pollution during the prehypertension (pre-HTN) stage could aggravate the progression from hypertension (HTN) to CVD, and consequent death. METHODS: A total of 168,010 adults with pre-HTN (120-139 mmHg systolic blood pressure or 80-89 mmHg diastolic blood pressure) from the UK Biobank were included in this analysis. We used a multistate model to explore the associations between five air pollutants (PM2.5, PM2.5 absorbance, PM10, NO2, and NOx) and the risk of six disease transitions (from pre-HTN to HTN, from pre-HTN to CVD, from pre-HTN to death, from HTN to CVD, from HTN to death, and from CVD to death). Mediation analyses were further conducted to explore the role of intermediate diseases in the dynamic progression of CVDs. RESULTS: During a median follow-up of 12 y, 13,743 (8.18%) of participants with pre-HTN developed HTN, whereas 12,825 (7.63%) and 4,467 (2.66%) directly developed CVD or died, respectively. Air pollution was positively associated with the dynamic disease progression. For example, a per-interquartile range increase of PM2.5 was significantly associated with the hazard ratios (HRs) of 1.105 [95% confidence intervals (CI): 1.083, 1.127], 1.045 (95% CI: 1.022, 1.068), and 1.086 (95% CI: 1.047, 1.126) in the transition from pre-HTN to HTN, CVD, and death, respectively. Higher levels of air pollution were associated with increased transition probability of disease progression. Mediation analyses indicated that intermediate diseases subsequently significantly mediated air pollutant-associated risk to develop more serious disease. CONCLUSIONS: This study provides evidence that air pollution might play a role in the early stages of CVD progression. Controlling air pollution might be an effective measure to prevent CVD progression and reduce the disease burden of CVD. https://doi.org/10.1289/EHP10967.
Subject(s)
Air Pollutants , Air Pollution , Cardiovascular Diseases , Hypertension , Prehypertension , Adult , Humans , Cardiovascular Diseases/epidemiology , Biological Specimen Banks , Particulate Matter/analysis , Air Pollution/analysis , Hypertension/epidemiology , Air Pollutants/analysis , United Kingdom/epidemiology , Disease Progression , Environmental Exposure/analysisABSTRACT
BACKGROUND AND OBJECTIVES: Studies on the effects of airborne particulates of diameter ≤ 1 µm (PM1), airborne particulates of diameter ≤ 2.5 µm (PM2.5) and airborne particulates of diameter ranges from 1 to 2.5 µm (PM1-2.5) on incidence of hyperuricemia are limited. We aimed to investigate the associations between PM1, PM2.5, and PM1-2.5 and hyperuricemia among male traffic officers. METHODS: We conducted a prospective cohort study of 1460 traffic officers without hyperuricemia in Guangzhou, China from 2009 to 2016. Exposures of PM1 and PM2.5 were estimated with a spatiotemporal model. PM1-2.5 concentrations were calculated by subtracting PM1 from PM2.5 concentrations. Cox's proportional hazards regressions models were used to examine the association between PM1, PM2.5, and PM1-2.5 and hyperuricemia, adjusted for potential confounders. Associations between PM1, PM2.5, and PM1-2.5 and serum uric acid (SUA) levels were evaluated with multiple linear regression models. RESULTS: Hazard ratios (HRs) and 95% confidence intervals (CIs) of hyperuricemia associated with 10 µg/m3 increment in PM1, PM2.5, and PM1-2.5 were 1.67 (95% CI:1.30-2.36), 1.49 (95% CI: 1.27-1.75), and 2.18 (95% CI: 1.58-3.02), respectively. The SUA concentrations increased by 12.23 µmol/L (95% CI: 5.91-18.56), 6.93 µmol/L (95% CI: 3.02-10.84), and 8.72 µmol/L (95% CI: 0.76-16.68) per 10 µg/m3 increase in PM1, PM2.5, and PM1-2.5, respectively. Stratified analyses indicated the positive associations of PM2.5 and PM1-2.5 with SUA levels were stronger in non-smokers, and PM1, PM2.5, and PM1-2.5 with SUA levels were stronger in non-drinkers. CONCLUSION: Long-term PM1, PM2.5, and PM1-2.5 exposures may increase the risk of hyperuricemia and elevate SUA levels among male traffic officers, especially in non-smokers and non-drinkers.
Subject(s)
Air Pollutants , Air Pollution , Hyperuricemia , Humans , Male , Particulate Matter/toxicity , Particulate Matter/analysis , Air Pollutants/analysis , Hyperuricemia/epidemiology , Prospective Studies , Uric Acid/analysis , Environmental Exposure/adverse effects , Environmental Exposure/analysis , China/epidemiology , Air Pollution/analysisABSTRACT
BACKGROUND: Previous studies on the association between ambient air pollution and cardiometabolic diseases (CMDs) focused on a single disease, without considering cardiometabolic multimorbidity (CMM) and the progression trajectory of CMDs. METHODS: Based on the UK Biobank cohort, we included 372,530 participants aged 37-73 years at baseline (2006-2010) with follow-up until September 2021. Incident CMDs cases were identified based on self-reported information and multiple health-related records in the UK Biobank. CMM was defined as the occurrence of at least two CMDs, including ischemic heart disease (IHD), stroke and type 2 diabetes (T2D). Exposure to ambient air pollutants, including particulate matter (PM) with aerodynamic diameter ≤2.5 µm (PM2.5), ≤10 µm (PM10), nitrogen dioxide (NO2), and nitrogen oxides (NOx) were estimated at participants' geocoded residential addresses based on the high-resolution (1 × 1 km) pollution data from 2001 to 2021 provided by UK Department for Environment, Food and Rural Affairs. Multi-state models with adjustment for potential confounders were used to examine the impact of long-term exposure to ambient air pollution on transitions from healthy to first CMD (FCMD), subsequently to CMM, and further to death. RESULTS: During a median follow-up of 12.6 years, 40,112 participants developed at least one CMD, 3896 developed CMM, and 21,739 died. Among the four pollutants, PM2.5 showed the strongest associations with all transitions from healthy to FCMD, to CMM, and then to death [hazard ratios (95 % confidence intervals) per interquartile range (IQR) increment: 1.62 (1.60, 1.64) and 1.68 (1.61, 1.76) for transitions from healthy to FCMD and from FCMD to CMM, and 1.62 (1.59, 1.66), 1.67 (1.61, 1.73), and 1.52 (1.38, 1.67) for death risk from healthy, FCMD, and CMM, respectively]. After dividing FCMDs into three specific CMDs, we found that ambient air pollution had differential impacts on disease-specific transitions within the same transition phase. CONCLUSIONS: Our findings indicate that there is potential for air pollution mitigation in contributing to the prevention of the development and progression of CMDs.
Subject(s)
Air Pollutants , Air Pollution , Diabetes Mellitus, Type 2 , Environmental Pollutants , Stroke , Humans , Prospective Studies , Incidence , Environmental Exposure/analysis , Air Pollution/analysis , Air Pollutants/analysis , Particulate Matter/analysis , Stroke/epidemiologyABSTRACT
BACKGROUND: Previous studies have revealed the relationship between cold spells and morbidity and mortality due to respiratory diseases, while the detrimental effects of cold spells on the length of hospital stay and hospitalization expenses remain largely unknown. METHODS: We collected hospitalization data for respiratory diseases in 11 cities of Shanxi, China during 2017-2019. In each case, exposure to meteorological variables and air pollution was estimated by the bilinear interpolation approach and inverse distance weighting method, respectively, and then averaged at the city level. Cold spells were defined as the daily mean temperature below the 10th, 7.5th, or 5th percentiles for at least 2 to 5 consecutive days. We applied distributed lag non-linear models combined with generalized additive models to assess cumulative effects and harvesting effects. RESULTS: There were significant associations between cold spells and hospital admissions, length of hospital stay, and hospital expenses for respiratory diseases. Compared with the non-cold spell period, the overall (lag 0-21) cumulative risk of hospitalization for total respiratory diseases was 1.232 (95 % CI: 1.090, 1.394) on cold spell days, and the increased length of hospital stay and hospitalization expenses were 112.793 (95 % CI: 10.755, 214.830) days and 127.568 (95 % CI: 40.513, 214.624) thousand Chinese yuan. The overall cumulative risks of cold spells on total respiratory diseases and pneumonia were statistically significant. We further observed harvesting effects in the associations between cold spells and hospital admission, length of hospital stay, and hospitalization expenses for respiratory diseases. CONCLUSIONS: Cumulative cold-spell exposure for up to three weeks is associated with hospitalization, length of hospital stay, and hospital expenses for respiratory diseases. The observed harmful effects of cold spells on respiratory diseases can be partly attributable to harvesting effects.
Subject(s)
Air Pollution , Respiration Disorders , Respiratory Tract Diseases , Humans , Length of Stay , Cold Temperature , Hospitalization , Respiratory Tract Diseases/epidemiology , China/epidemiology , HospitalsABSTRACT
BACKGROUND: To estimate the associations between ambient particulate matter (PM) pollution of different sizes (PM1, PM2.5, and PM10) and risk of rehospitalization among stroke patients, as well as the attributable burden in China. METHODS: We built a cohort of 1,066,752 participants with an index stroke hospitalization in Sichuan, China from 2017 to 2019. Seven-day and annual average exposures to PM pollution prior to the date of the index hospitalization were linked with residential address using a bilinear interpolation approach. Cox proportional hazard models were constructed to assess the association between ambient PM and the risk of rehospitalization. The burden of stroke rehospitalization was estimated using a counterfactual approach. RESULTS: 245,457 (23.0 %) participants experienced rehospitalization during a mean of 1.15 years (SD: 0.90 years) of follow-up. Seven-day average concentrations of PM were associated with increased risk of rehospitalization: the hazard ratios (HRs) per 10 µg/m3 were 1.034 (95 % confidence interval [CI]: 1.029-1.038) for PM1, 1.033 (1.031-1.036) for PM2.5, and 1.030 (1.028-1.031) for PM10; the hazard ratios were larger for annual average concentrations: 1.082 (1.074-1.090) for PM1, 1.109 (1.104-1.114) for PM2.5, and 1.103 (1.099-1.106) for PM10. The associations were stronger in participants who were female, of minority ethnicity (non-Han Chinese), who suffered from an ischemic stroke, and those admitted under normal conditions. Population attributable fractions for stroke rehospitalization ranged from 4.66 % (95 % CI: 1.69 % to 7.63 %) for the 7-day average of PM1 to 17.05 % (14.27 % to 19.83 %) for the annual average of PM10; the reducible average cost of rehospitalization per participant attributable to PM ranged from 492.09 (178.19 to 806) RMB for the 7-day average of PM1 to 1801.65 (1507.89 to 2095.41) RMB for the annual average of PM10. CONCLUSIONS: Ambient PM pollution may increase the risk of rehospitalization in stroke patients and is responsible for a significant burden of stroke rehospitalization.