ABSTRACT
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.
Subject(s)
Seizures , Sleep Wake Disorders , Child , Humans , Surveys and Questionnaires , Cities , China/epidemiology , Sleep Wake Disorders/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
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: Previous studies have indicated that chlorinated polyfluorinated ether sulfonic acids (Cl-PFESAs), when used as an alternative to per- and polyfluoroalkyl substances (PFASs), result in kidney toxicity. However, their co-exposure with heavy metals, has not yet been described. OBJECTIVES: To explore the joint effects of Cl-PFESAs and heavy metal exposure on renal health in Chinese adults, and identify specific pollutants driving the associations. METHODS: Our sample consists of 1312 adults from a cross-sectional survey of general communities in Guangzhou, China. We measured Cl-PFESAs, legacy PFASs (perfluorooctanoic acid [PFOA] and perfluorooctane sulfonated [PFOS]), and heavy metals (arsenic, cadmium, and lead). The relationship between single pollutant and glomerular filtration rate (eGFR) and the odds ratio (OR) of chronic kidney disease (CKD) was studied using Generalized additive models (GAMs). Bayesian Kernel Machine Regression (BKMR) models were applied to assess joint effects of Cl-PFESAs and heavy metals. Additionally, we conducted a sex-specific analysis to determine the modification effect of this variable. RESULTS: In single pollutant models, CI-PFESAs, PFOA, PFOS and arsenic were negatively associated with eGFR. Additionally, PFOA and heavy metals were positively correlated with the OR of CKD. For example, the estimated change with 95% confidence intervals (CI) of eGFR at from the highest quantile of 6:2 Cl-PFESA versus the lowest quantile was -5.65 ng/mL (95% CI: -8.21, -3.10). Sex played a role in modifying the association between 8:2 Cl-PFESA, PFOS and eGFR. In BKMR models, pollutant mixtures had a negative joint association with eGFR and a positive joint effect on CKD, especially in women. Arsenic appeared to be the primary contributing pollutant. CONCLUSION: We provide epidemiological evidence that Cl-PFESAs independently and jointly with heavy metals impaired kidney health. More population-based human and animal studies are needed to confirm our results.
Subject(s)
Alkanesulfonic Acids , Arsenic , Environmental Pollutants , Fluorocarbons , Renal Insufficiency, Chronic , Adult , Animals , Female , Humans , Alkanesulfonic Acids/analysis , Arsenic/toxicity , Arsenic/analysis , Cross-Sectional Studies , Bayes Theorem , Sulfonic Acids/analysis , Ethers , Ether , China/epidemiology , Alkanesulfonates/analysis , Environmental Pollutants/toxicity , Environmental Pollutants/analysis , Fluorocarbons/toxicity , Fluorocarbons/analysis , Cadmium/analysis , KidneyABSTRACT
BACKGROUND: Although ozone exposure has neurological toxicity, it remains unclear whether it was associated with an increased risk of attention-deficit/hyperactivity disorders (ADHD) among childhood. METHODS: We matched the four-year average ozone concentration with questionnaire data for 35,103 children aged 3-12 years from seven cities in Liaoning, China, 2012-2013. Using mixed-effect logistic regression models, we assessed the association of ozone concentration with multiple ADHD indicators using the Conners Abbreviated Symptom Questionnaire (C-ASQ), including explicit attention-deficit/hyperactivity symptoms (ADHD; score ≥15), attention-deficit/hyperactivity disorder tendencies (ADHD-T; 11 ≤ score ≤14), and attention-deficit/hyperactivity problems (ADHP; score ≥11). Results were also stratified by sociodemongraphics. RESULTS: After adjusting for covariates, we found that each interquartile range (IQR) increase in ozone concentration was associated with an increased risk of ADHD, ADHD-T, and ADHP (P < 0.001) with an odds ratio of 1.12 (95% confidence interval, 1.04-1.21), 1.08 (1.03-1.13), and 1.09 (1.05-1.14), respectively. Additionally, we found greater effect estimates in children who reported longer exercise time (vs those with limited exercise time) with odds ratio of 1.18 (1.07-1.31) vs 1.06 (0.96-1.17) for ADHD, 1.13 (1.06-1.21) vs 1.03 (0.96-1.10) for ADHD-T, and 1.15 (1.08-1.21) vs 1.04 (0.98-1.10) for ADHP. Non-breastfed children were also shown to be more vulnerable to ADHD with an odds ratio of 1.22 (1.09-1.36) compared with 1.06 (0.96-1.16) among the rest. CONCLUSIONS: Long-term ozone exposure may be associated with increased ADHD among children. Additional studies are needed to validate our findings and support policies and interventions to address this growing public health concern.
Subject(s)
Attention Deficit Disorder with Hyperactivity , Ozone , Child , Humans , Attention Deficit Disorder with Hyperactivity/chemically induced , Attention Deficit Disorder with Hyperactivity/epidemiology , Odds Ratio , Surveys and Questionnaires , Attention , Ozone/toxicityABSTRACT
Individuals with cardiovascular disease (CVD) are particularly vulnerable to dementia, but it remains unclear whether air pollution exposure links with higher risk of dementia among those with CVD. The data were derived from the UK Biobank study (UKB). Dementia-free participants with CVD at baseline were included. Air pollution exposure was assessed through land use regression models, including particulate matter (PM2.5, PM2.5-10, and PM10), nitrogen dioxide (NO2), and nitrogen oxides (NOX). A Cox proportional hazards model was used to investigate the associations between air pollution exposure and incident dementia among individuals with CVD. Air pollution was associated with dementia among individuals with CVD, and the hazard ratios of dementia associated with each interquartile range (IQR) µg/m3 increase in air pollution were 1.07 (95% CI: 1.02, 1.12) for PM2.5, 1.10 (95% CI: 1.04, 1.15) for PM10, 1.08 (95% CI: 1.03, 1.14) for NO2 and 1.05 (95% CI: 1.00, 1.09) for NOx. Associations between air pollution and all-cause dementia were found to be significant among individuals with hypertension. Adverse effects of air pollution were also observed for Alzheimer's dementia (AD) and vascular dementia (VaD), with a higher effect for AD. Observed associations remained similar in subgroups of APOE ε4 carriers and noncarriers, although there was a higher risk difference across different air pollution concentration among these individuals carrying APOE ε4. Air pollution emerges as a critical risk factor for dementia among individuals with CVD, regardless of genetic susceptibility indicated by the APOE genotype. Notably, individuals with hypertension might be susceptible to the adverse effects of air pollution, leading to a higher incidence of dementia. Understanding these impacts on dementia among individuals with CVD may promote better targeted prevention and clinical management strategies.
Subject(s)
Air Pollutants , Air Pollution , Alzheimer Disease , Cardiovascular Diseases , Hypertension , Humans , Cardiovascular Diseases/epidemiology , Cardiovascular Diseases/genetics , Cardiovascular Diseases/chemically induced , Air Pollutants/analysis , Nitrogen Dioxide/analysis , Longitudinal Studies , Apolipoprotein E4 , Environmental Exposure/adverse effects , Environmental Exposure/analysis , Air Pollution/adverse effects , Air Pollution/analysis , Particulate Matter/analysis , Hypertension/chemically induced , GenotypeABSTRACT
BACKGROUND: With increased applications of rare earth elements (REEs) across various industries, evaluating the relationship between REEs exposure and potential health effects has become a public concern. In vivo experiments have established that REEs impact renal function. However, relevant epidemiological evidence on this relationship remains scarce. The objective of this study is to examine the impact of exposure to REEs on renal function. METHODS: In this cross-sectional study, 1052 participants were recruited from Guangxi, China. We measured urinary concentrations of 12 REEs using an inductively coupled plasma-mass spectrometer (ICP-MS). Multiple linear regression models were developed to explore the relationship between a single REEs exposure and the estimated glomerular filtration rate (eGFR), a marker of renal function. Weighted quantile sum (WQS) regression and Bayesian kernel machine regression (BKMR) were used to examine the combined effects of REE co-exposure on eGFR. RESULTS: In the multiple linear regression analysis, increasing the concentrations of lanthanum (La, ß: 8.22, 95% CI: 5.67-10.77), cerium (Ce, ß:6.61, 95% CI: 3.80-9.43), praseodymium (Pr, ß: 8.46, 95% CI: 5.85-11.07), neodymium (Nd, ß:8.75, 95% CI: 6.10-11.41), and dysprosium (Dy, ß:7.38, 95% CI: 4.85-9.91) significantly increased the eGFR. In the WQS regression model, the WQS index was significantly associated with eGFR (ß: 4.03, 95% CI: 2.46-5.60), with Pr having the strongest correlation with eGFR. Similar results were obtained in the BKMR model. Additionally, interactions between Pr and La, and Pr and Nd were observed. CONCLUSIONS: Co-exposure to REEs is positively associated with elevated eGFR. Pr is likely to have the most significant influence on increased eGFRs and this might be exacerbated when interacting with La and Nd. Mixed exposure to low doses of REEs had a protective effect on renal function, which can provide some evidence for the exposure threshold of REEs in the environment. TRIAL REGISTRATION: The study has been approved by the Guangxi Medical University Medical Ethics Committee (#20170206-1), and all participants provided written informed consent.