Potential Effect Modifiers Research Articles

Exploring cognitive overload in adults with visual impairment: The association between concentration and fatigue.

This research contributes to the concept of cognitive overload and the association between concentration and fatigue in individuals with visual impairment (VI). Gaining more insight into these and other factors explaining cognitive overload is essential for a better understanding, prevention, and treatment of fatigue severity in individuals with VI. Individuals with VI need to use additional cognitive resources to compensate for their loss of vision. These cognitive demands include increased concentration, which may put an extra burden on energy levels. This study aimed to expand upon previous research on the concept of cognitive overload by exploring the relationship between concentration and fatigue severity in individuals with VI. A cross-sectional study was conducted based on data from the eligibility screening of the E-nergEYEze trial (n = 213). Concentration problems were measured with the Checklist of Individual Strengths subscale Concentration, and fatigue severity was measured with the Checklist of Individual Strengths subscale Fatigue Severity. Linear regression analyses were performed to investigate the association between concentration problems and fatigue severity. Potential effect modifiers (i.e., sociodemographic and vision-related characteristics) were considered, and associations were corrected for confounding. Concentration problems were directly and positively associated with fatigue severity (β = 0.47; R2 = 0.10; 95% confidence interval, 0.28 to 0.66; adjusted model: β = 0.52; R2 = 0.16; 95% confidence interval, 0.32 to 0.72). No relevant effect modifiers were identified. However, other factors that were not included in this study were involved in this association. This study contributes to understanding the cognitive overload as experienced by adults with VI and highlights the importance of the association of concentration problems, as a reflection of the cognitive burden and perceived fatigue. It is recommended to identify and address concentration difficulties through suitable awareness and treatment strategies to prevent and reduce severe fatigue in this population.

Vitamin D status, physical activity and long-term mortality risk after myocardial infarction: a prospective analysis in the Alpha Omega Cohort.

In post-myocardial infarction (MI) patients, we examined independent and combined associations of vitamin D status and physical activity (PA) with long-term mortality, including effect modification by health determinants. We conducted a prospective analysis of 4,837 MI patients from the Alpha Omega Cohort. Baseline blood samples (2002-2006) were assessed for plasma 25-hydroxyvitamin D (25[OH]D) levels using LC-MS/MS. PA was assessed using a validated questionnaire. Patients were followed for mortality through December 2022. HRs for CVD and all-cause mortality were obtained across sex-specific tertiles of 25(OH)D and four categories of PA using Cox models, adjusted for sociodemographic and lifestyle factors. Potential effect modification by health determinants was examined through stratification. Patients were 69±5.6 years old, 78% was male, 21% had diabetes, and 10% used vitamin D-containing supplements. Over 14.4 years, 3,206 deaths occurred, including 1,244 from CVD. Median 25(OH)D was 21.1 ng/mL and 44% was vitamin D deficient (<20 ng/mL). Higher 25(OH)D levels were associated with lower CVD (HR:0.63, 95%CI:0.54,0.74) and all-cause mortality (HR:0.68, 95%CI:0.62,0.75). For PA levels (high vs. light), HRs were 0.72 (95%CI:0.61,0.85) for CVD mortality and 0.83 (95%CI:0.75,0.92) for all-cause mortality. Patients with low 25(OH)D and no PA had a threefold higher mortality risk than those with high 25(OH)D levels and high PA. The associations were not significantly modified by sex, comorbidities and other health determinants. Vitamin D status and PA were inversely and independently associated with long-term risk of CVD and all-cause mortality after MI, regardless of other health determinants.

The effect and burden of sand-dust storms on asthma hospitalization: Evidence from cities with arid climate in China

Evidence concerning the impact of sand-dust storms (SDS) on asthma is limited, and little is known about the associated public health burden, especially in regions with arid climates. Therefore, this study seeks to evaluate the effect of SDS on asthma hospitalization and quantify the associated hospital and economic burden in a province with typical arid climates. We collected provincial asthma hospitalization, air pollutants and meteorological data of 14 cities in Gansu province. The space-time-stratified case-crossover design combined with a conditional quasi-Poisson regression was used to estimate the association between SDS and asthma hospitalization during 2018-2022. We further explored the interactive effect of SDS and low temperature, and explored potential effect modifications of gender, age, seasons and regions by stratified analyses. Finally, we calculated the hospital and economic burden of asthma attributed to SDS. A total of 54,134 hospitalization records for asthma and 791 SDS events were recorded during the study period. Northwestern area with arid climate displayed more frequent SDS events and asthma hospitalization compared with regions with subtropical or temperate monsoon climate. The relative risk (RR) of asthma hospitalization increased with SDS, with the greatest RR at lag1, which was 1.164 with a 95% confidence interval (CI) of 1.101 to 1.231. We further found that low temperature had an interactive effect with SDS to trigger asthma hospitalization. Stronger associations were observed in males, school-aged children, cold season and northwestern area. The total fraction of asthma hospitalization attributable to SDS was 1.64 % (95% CI: 1.06% to 2.18%), and a conservative estimate of relative healthcare costs was 4.49 (95% CI: 2.92 to 5.99) million China Yuan. Our findings suggest the necessity of controlling SDS and implementing region-specific public health policies as well as personal protective measures against SDS.

The associations between exposure to ambient air pollution and coagulation markers and the potential effects of DNA methylation

Previous studies have illustrated the pivotal role of coagulation biomarkers in the link between air pollution and cardiovascular disease (CVD). However, inconsistencies remain in the conclusions, with limited studies conducted in rural areas of China. We conducted a panel study in rural areas of Henan Province, China. Considering the potential effect modifications of atherosclerotic cardiovascular disease (ASCVD) risks, 104 participants were enrolled, comprising two matched groups: 52 with high ASCVD risks and 52 with low ASCVD risks. DNA methylation at CpG sites and coagulation indices were measured for all participants. Linear mixed-effect regression models were used to evaluate the associations between ambient air pollution, coagulation biomarkers, and DNA methylation. We observed that for every 5-day standard deviation (SD) increment of PM2.5 (11.91μg/m³) and PM10 (13.65μg/m³), fibrinogen increased by 7.70% (95%CI: 2.27, 13.12) and 8.50% (95%CI: 2.46, 14.55), respectively. SO2 (6.95μg/m³) was associated with 40.25% (95%CI: 14.83, 65.67) increase in plasminogen activator inhibitor-1 (PAI-1). Decreased methylation at CpG sites was associated with exposure to air pollution. However, DNA methylation did not mediate the association between ambient air pollution and coagulation. Our study revealed the harmful impact of ambient air pollution on coagulation function but found no significant mediation effects of DNA methylation.

The community food environment as an effect modifier of the relationship between racial discrimination and food insecurity among adults in Southern Brazil

BackgroundRacial discrimination is linked to unhealthy food environments and a higher prevalence of food insecurity. However, no study has explored their interrelated effects. We analyzed the relationship between racial discrimination, community food environment, and food insecurity in adults of different socioeconomic status. We also investigated the potential modifying effect of the food environment on the relationship between racism and food insecurity.MethodsThis was a cross-sectional study of 400 adults aged 20–70 years residing in the central area of ​​Porto Alegre, the capital of Rio Grande do Sul state. Race and racial discrimination were assessed by self-reported race/skin color using the Experiences of Discrimination scale (EOD), respectively. The food environment was assessed using the Nutrition Environment Measures Survey in Stores (NEMS-S) tool. Food insecurity was assessed using the short version of the Brazilian Food Insecurity Scale (EBIA for short, in Portuguese). Poisson regression with robust variance was employed for the multivariate analysis.ResultsThe prevalence of food insecurity was higher in areas with a poorer food environment (areas 1 and 3; 56.6% and 58.8%, respectively). Racial discrimination was associated with food insecurity, where every 1-point increase in the racial discrimination score increased the likelihood of food insecurity by 7% (prevalence ratio [PR] 1.07; 95% CI, 1.03–1.20). When stratifying the analyses by food environment, racial discrimination was associated with food insecurity only in areas with a poorer food environment (PR 1.06; 95% CI, 1.01–1.10).ConclusionsExperiences of racial discrimination were associated with a higher prevalence of food insecurity in the study population. The community food environment was an effect modifier of this relationship, highlighting the relevance of interventions in the food environment focused on areas with a greater presence of Black people as a way of combating racism and food insecurity.

Short-term effects of ambient temperature variability on myocardial infarction hospitalizations in Sweden: A nationwide case-crossover study

Abstract Background Climate change threatens human health and general welfare via multiple dimensions. However, the short-term effect of temperature variability, a crucial aspect of climate change, on myocardial infarction (MI) remains largely unexplored. Purpose We aimed to assess the short-term effects of temperature variability on MI hospitalizations within the nationwide SWEDEHEART registry. Methods This population-based nationwide study involved 228,897 MI patients from the SWEDEHEART registry in Sweden from 2005 to 2019. High-resolution (1 km × 1 km) daily mean ambient temperature was estimated using a spatiotemporal machine learning methodology and assigned to patients’ home addresses. Temperature variability was calculated as the difference between the same-day (as the MI event) ambient temperature and the average temperature recorded over the preceding seven days. Specifically, an upward temperature shift represents a rise in the current day’s temperature relative to the seven-day average, while a downward temperature shift indicates a corresponding decrease. A time-stratified case-crossover design incorporating a conditional logistic regression model with distributed lag non-linear model was applied to estimate the association between ambient temperature variability and total MI, ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI). Moreover, we assessed potential effect modification by sex and medication intake. The results were expressed as odds ratio (OR, with their 95% confidence intervals [CIs]) per 1°C increase in temperature variability. Results Our study found that a 1°C increase in upward temperature shift was significantly associated with increased risks for total MI, STEMI, and NSTEMI (OR [95% CI]: 1.010 [1.006-1.015], 1.014 [1.006-1.022], and 1.009 [1.004-1.014], respectively). Furthermore, a 1°C greater in downward temperature shift was significantly associated with decreased risks for total MI and NSTEMI (OR [95% CI]: 0.995 [0.991-0.999], and 0.993 [0.988-0.998], respectively). Moreover, we found that males and patients who were on any heart medication, particularly digitalis, were at a higher risk of MI associated with exposure to higher upward temperature shifts compared to females and their counterparts not taking these medications. Conclusions This nationwide case-crossover study provides novel evidence that short-term exposure to increasing upward temperature shift is associated with an increased risk of MI hospitalization. Our finding highlights the cardiovascular health threats posed by upward temperature shifts, which are anticipated to increase in frequency and intensity due to climate change.

Imaging predictors of adverse prognosis in fabry disease cardiomyopathy: a systematic review and meta-analysis

Abstract Background Cardiac involvement represents the main cause of death in patients with Fabry disease (FD). Echocardiography and Cardiac Magnetic Resonance (CMR) have an established diagnostic role, but their prognostic value remains unresolved. This systematic review and meta-analysis sought to assess the prognostic implications of imaging parameters in FD. Methods PubMed, ClinicalTrials.gov, Embase and Cochrane Library databases were searched for studies published from inception through to October 1, 2023. Full-length original papers including FD patients undergoing baseline imaging assessment and clinical follow-up were selected. Pre-defined study outcomes were a cardiovascular endpoint and a composite clinical endpoint. A meta-analysis of the studies investigating the effect of single imaging parameters on a pre-specified cardiovascular endpoint and a separate analysis on a pre-specified composite clinical endpoint were performed to obtain the pooled estimates for the association between the imaging parameters and the study outcome. The study protocol was registered in PROSPERO. Results Thirteen studies including 1,399 FD patients (44.8% males) were selected. At pooled analysis, late gadolinium enhancement (HR 4.39; 95% CI 2.5-7.71), left atrium volume indexed (HR 1.02 per ml/m2; 95% CI 1.01-1.04), E/e’ (HR 1.14 per unit increase; 95% CI 1.08-1.21), left ventricular (LV) mass indexed (HR 1.014 per mg/m2; 95% CI 1.006-1.023), maximum LV wall thickness (HR 1.19 per mm, 95% CI 1.04-1.36), LV-global longitudinal strain (HR 1.2 per unit increase; 95% CI 1.2-1.27), were significantly associated with the cardiovascular endpoint, whereas T1-mapping (p=0.115) and LV-ejection fraction (p=0.305) were not. T1-mapping was associated with the composite endpoint (HR 0.986 per msec increase; 95% CI 0.976-0.997). Meta-regression analysis did not show any significant interaction between each of the potential effect modifiers. Conclusion This meta-analysis demonstrates a robust prognostic value regarding several imaging parameters in FD, specifically indexes of LV mass and wall thickness, diastolic dysfunction, LV-GLS, and LGE presence. These findings support multimodality cardiovascular imaging, including CMR, in FD disease patients to predict long-term prognosis and call for longitudinal multicentre studies to develop multi-modality-imaging derived risk-score algorithms.

Modifying effect of obesity status on the association between low-density lipoprotein cholesterol with incident hemorrhagic stroke: evidence from a community-based longitudinal cohort study in China

Abstract Background Previous results on the association between lipids and hemorrhagic stroke were controversial. Modifying effect of obesity on the association between low-density lipoprotein cholesterol (LDL-C) and hemorrhagic stroke risk in the Chinese community-based population remains unclear. Objectives We aimed to investigate the association between LDL-C and hemorrhagic stroke risk in the Chinese community-based population. In addition, we aimed to explore the potential modifying effect of obesity status, particularly abdominal obesity, on this relationship. Methods A total of 7899 eligible subjects, without history of stroke and myocardial infarction, and any use of lipid-lowering medication at baseline, were enrolled in this study. Levels of LDL-C, total cholesterol (TC), triglyceride (TG), and high-density lipoprotein cholesterol (HDL-C) were assessed at baseline. The primary endpoint was the hemorrhagic stroke. Abdominal obesity was defined as waist circumference &amp;gt; 90 cm in men and &amp;gt; 85 cm in women. Results Of all participants, the mean age was 56.13 ± 8.87 years, 2848 (36.1%) were male. During a mean 9.71-year follow-up, 66 hemorrhagic strokes occurred. After multivariable adjustment (Figure 1), compared to participants with LDL-C levels 2.6 – 3.4 mmol/L, those with LDL-C levels &amp;lt; 1.8 mmol/L had 3.32 times the risk (hazard ratio [HR]: 3.32; 95% confidence interval [CI]: 1.24, 8.84) of incident hemorrhagic stroke. Compared with participants with TC levels 3.1 – 5.2 mmol/L, HR (95% CI) was 7.82 (2.36, 25.90) for hemorrhagic stroke in those with TC &amp;lt; 3.1 mmol/L. We observed no significant associations between TG or HDL-C levels and hemorrhagic stroke risk. Interaction effects were found between obesity and LDL-C for incident hemorrhagic stroke. Accordingly, significant associations between low LDL-C level (&amp;lt; 1.8 mmol/L) and the risk of incident hemorrhagic stroke were found only among abdominal obesity participants (HR: 3.76; 95% CI: 1.01, 13.97), or those with body mass index (BMI) &amp;gt; = 24 kg/m2 (HR: 3.74; 95% CI: 1.24, 11.34) (Figure 2). Conclusions LDL-C levels &amp;lt; 1.8mmol/L and TC levels &amp;lt; 3.1mmol/L were associated with increased risk of hemorrhagic stroke. Modifying effect of obesity status on the association between low LDL-C level and hemorrhagic stroke was observed in our study.

Modification of the association between coffee consumption and constipation by alcohol drinking: A cross-sectional analysis of NHANES 2007-2010.

The association between coffee consumption and constipation remains unclear. This study aimed to examine the relationship of coffee consumption with the risk of constipation, while also investigating potential effect modifiers. This cross-sectional study included 7844 participants from the National Health and Nutrition Examination Survey (NHANES) 2007-2010. Coffee consumption was extracted from the 24-hour dietary recall. Constipation was assessed using the Bristol Stool Form Scale. The association between coffee consumption and constipation was assessed using multivariable restricted cubic spline and logistic regression with odds ratio (OR) and 95% confidence interval (CI). There was a J-shaped relationship between total coffee consumption and the risk of constipation in the whole population (p for nonlinearity = 0.049), with 1-2 cups/day of total coffee potentially reducing the risk of constipation by 39% (OR 0.61, 95% CI 0.35-1.06, p = 0.07). As for caffeinated coffee, a J-shaped association between its consumption and the risk of constipation was also observed in the whole population (p for nonlinearity = 0.008), with 1-2 cups/day being significantly associated with a reduced risk (OR 0.57, 95% CI 0.35-0.95, p = 0.03). When restricting to never drinkers of alcohol, the associations between total and caffeinated coffee consumption and constipation shifted to inverse linear trends, where at least 3 cups/day was significantly associated with an 88% reduction in constipation risk (total coffee: OR 0.12, 95% CI 0.02-0.68, p = 0.02; caffeinated coffee: OR 0.12, 95% CI 0.02-0.70, p = 0.02). Decaffeinated coffee showed no association with constipation. Consuming 1-2 cups of caffeinated coffee daily was associated with a reduced risk of constipation in the general population. Among never drinkers of alcohol, a linear protective effect was observed, with a notable 88% reduction in constipation risk for those consuming at least 3 cups per day. Moderate caffeinated coffee intake may therefore be a viable dietary strategy for managing constipation in the general population.

Regular cannabis smoking and carotid artery calcification in the Multi-Ethnic Study of Atherosclerosis (MESA).

Studies on cannabis use and adverse cardiovascular outcomes have reported conflicting results. Research on its relationship to calcified arterial plaque remains limited. Cross-sectional data from 2152 participants at Exam 6 (2016-2018) in the Multi-Ethnic Study of Atherosclerosis (MESA) were analyzed, including self-reported cannabis smoking patterns and carotid artery calcification (CAC) as measured via computed tomography. Multivariable relative and absolute risk regression models were used to estimate adjusted prevalence ratios (PRs) and prevalence differences, respectively, for the presence of calcified plaque. Multivariable linear regression was then used to compare group differences in the extent of CAC in those with calcified plaque. A minority of participants (n = 159, 7.4%) reported a history of regular cannabis smoking. Among all participants, 36.1% (n = 777) had detectable CAC. In models adjusted for demographics, behavioral, and clinical cardiovascular disease factors, a history of regular cannabis smoking was not associated with the prevalence of CAC in either common carotid artery (PR: 1.14, 95% CI: 0.88 to 1.49). In the subset of participants with calcified plaque, and in separate fully adjusted multivariable linear regression models, a history of regular cannabis smoking was not associated with increased calcium volume (difference = 7.7%, 95% CI: -21.8 to 48.5), calcium density (difference = 0.4%, 95% CI: -6.6 to 7.9), or Agatston score (difference = 32.1%, 95% CI: -31.8 to 155.8) in either carotid artery. Models exploring potential effect modification by age, race/ethnicity, and tobacco smoking status showed no significant association, except for higher CAC prevalence in men with a history of regular cannabis smoking. In a racially and ethnically diverse cohort of older adults with a moderately high prevalence of CAC, no associations were found between a history of regular cannabis smoking, duration, or recency of cannabis smoking, and the prevalence of carotid calcified plaque. These findings were consistent across age, race/ethnicity, and cigarette smoking, except for an increased prevalence in men with a history of regular cannabis smoking. Similarly, in a subgroup with CAC, no association was found between a history of regular cannabis smoking and extent of calcification as measured by volume, density, and Agatston score.

Adherence to lifelines diet is associated with lower lung cancer risk in 98,459 participants aged 55 years and above: a large prospective cohort study.

Lifelines Diet Score (LLDS) was developed based on the 2015 Dutch Dietary Guidelines and current international scientific evidence. As a dietary quality assessment tool, the LLDS aims to evaluate the association between the Lifeline diet and the risk of chronic diseases. However, the evidence linking LLDS to lung cancer risk is currently limited. Our objective was to explore whether adherence to the LLDS is associated with reduced incidence and mortality of lung cancer, including its major histological subtypes: small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC). Data for this research were sourced from the Prostate, Lung, Colorectal, and Ovarian (PLCO) Trial. The LLDS for each participant was calculated based on responses to the dietary history questionnaire (DHQ), and subsequently analyzed after being categorized into quintiles. The Cox proportional hazards regression model was utilized to compute the hazard ratios (HRs) and 95% confidence intervals (CIs) for both the incidence and mortality of lung cancer, SCLC and NSCLC. Additionally, stratified analyses were conducted to ascertain possible effect modifiers, and several sensitivity analyses were performed to evaluate the robustness of the findings. During the mean follow-up periods of 8.8 years for incidence and 15.1 years for mortality, we identified 1,642 new cases and 1,172 related deaths from lung cancer. Participants in the highest quartiles of LLDS compared to those in the lowest exhibited a reduced incidence (HRQ4:Q1 = 0.80, 95% CI = 0.68-0.94, P for trend = 0.003) and mortality (HRQ4:Q1 = 0.81, 95%CI = 0.67-0.98, P for trend = 0.009) of lung cancer. Furthermore, this negative association remained for SCLC incidence (HRQ4:Q1 = 0.55, 95% CI = 0.35-0.87, P for trend = 0.002) and mortality (HRQ4:Q1 = 0.42, 95% CI = 0.25-0.70, P for trend <0.001). The association between LLDS and the incidence and mortality of lung cancer is not influenced by pre-defined potential effect modifiers (all P interaction > 0.05). The sensitivity analyses substantiated the robustness of the results. In conclusion, our research indicates that among 98,459 U.S. adults aged 55 and older, adherence to the LLDS is linked to a diminished incidence and mortality of lung cancer.

The association between brominated flame retardants exposure with Parkinson's disease in US adults: a cross-sectional study of the National Health and Nutrition Examination Survey 2009-2016.

Increasing evidence suggests that environmental factors play a crucial role in the pathogenesis of Parkinson's disease (PD). Humans are simultaneously exposed to multiple brominated flame retardants (BFRs) in the environment. However, the relationship between BFRs and PD remains unclear. This study was designed to investigate the overall association between BFRs and PD in a nationally representative US population and to further identify significant chemicals. This study used data from 7,161 NHANES participants from 2009 through 2016. The serum BFRs registry included PBDE-28, PBDE-47, PBDE-85, PBDE-99, PBDE-100, PBDE-153, PBDE-154, PBDE-183, PBDE-209, and PBB-153. A survey-weighted generalized logistic regression model with restricted cubic splines (RCS) was used to evaluate the association between single BFRs exposure and periodontitis. Meanwhile, weighted quantile sum (WQS) regression and Bayesian kernel machine regression (BKMR) were used to evaluate the overall association of mixed frankincense powder with periodontitis and to identify significant chemicals. Sensitivity analysis was performed to evaluate the robustness of the results. Among the 7,161 participants, 65 had PD. PD patients were older (mean age 57.79 vs. 46.57 years) and had a higher proportion of females (70.86%) compared to non-PD participants. Serum levels of PBB-153 were significantly higher in those with PD. Logistic regression analyses revealed a non-linear, inverted U-shaped relationship between serum PBB-153 and PD risk. The risk of PD increased with higher PBB-153 levels up to the 3rd quartile (Q3), beyond which the risk declined (Q3 vs. Q1: OR = 4.98, 95% CI = 1.79-13.86; Q4 vs. Q1: OR = 3.23, 95% CI = 1.03-10.08). PBB-153 (43.40%), PBDE-153 (24.75%), and PBDE-85 (19.51%) contributed most to the weighted quantile sum index associated with PD risk. Bayesian kernel machine regression confirmed the inverted U-shaped dose-response pattern for PBB-153 and the overall BFR mixture. Restricted cubic spline analyses corroborated the non-linear relationship between PBB-153 and PD, which was more pronounced among women and those aged 37-58 years. Sensitivity analyses substantiated these findings. This nationally representative cross-sectional study revealed a novel non-linear, inverted U-shaped relationship between serum levels of the brominated flame retardant PBB-153 and Parkinson's disease risk in U.S. adults. The risk increased with higher PBB-153 exposure up to a point, beyond which it declined. This complex dose-response pattern highlights the importance of considering potential hormetic mechanisms and effect modifiers when evaluating environmental exposures and neurodegenerative diseases. Further research is warranted to elucidate the underlying biological pathways and inform risk mitigation strategies.

Prolonged exposure to air pollution and risk of acute kidney injury and related mortality: a prospective cohort study based on hospitalized AKI cases and general population controls from the UK Biobank

BackgroundPrevious investigations identified a connection between air pollution and kidney diseases. Nevertheless, there is a lack of comprehensive evidence on the long-term risks posed by air pollution with respect to acute kidney injury (AKI) and AKI-related death.MethodsThis prospective cohort analysis included 414,885 UK Biobank (UKB) participants who did not exhibit AKI at the study’s outset. AKI was defined based on ICD-10 codes recorded for hospitalized patients. Cox proportional hazards models were used to assess the association between prolonged exposure to air pollutants (particulate matter with diameters of 2.5 micrometers or less (PM2.5), between 2.5 and 10 micrometers (PM2.5−10), and 10 micrometers or less (PM10), along with nitrogen dioxide (NO2) and nitrogen oxides (NOx)) and the risk of AKI and AKI-related death, adjusting for potential confounders including sex, age, ethnicity, education, income, lifestyle factors, and relevant clinical covariates. Restricted cubic splines were applied to evaluate non-linear dose-response relationships, and stratified analyses were performed to explore potential effect modification across subgroups.ResultsOver an average follow-up duration of 11.7 years, 14,983 cases of AKI and 326 cases of AKI-related death were diagnosed. Quartile analysis showed individuals exposed to higher levels of these air pollutants had a significantly higher risk of developing AKI and AKI-related death compared to those in the lowest quartile (all P < 0.05). The RCS curves depicting the relationship between PM2.5, PM2.5−10, PM10, NO2, NOx, and the risk of AKI showed a significant departure from linearity (P for non−linearity < 0.05), while the relationships between PM2.5, NO2, NOx, and the risk of AKI-related death did not exhibit a significant departure from linearity (P for non−linearity > 0.05). Sensitivity analyses confirmed the robustness of our findings.ConclusionOur study reveals a direct association between prolonged air pollution exposure and elevated risks of both AKI and AKI-related death. These findings offer scientific validation for the adoption of environmental and public health measures directed towards the reduction of air pollution. Such initiatives could potentially ease the impact associated with AKI and AKI-related death.

Childhood exposure to air pollution, noise, and surrounding greenness and incident hypertension in early adulthood in a US nationwide cohort–the Growing Up Today Study (GUTS)

Exposure to increased air pollution, noise, and reduced surrounding greenness have been suggested as potential environmental risk factors for hypertension in adults, but limited evidence exists regarding early-life exposure, particularly from prospective studies. We investigated independent and joint associations of childhood exposure to these factors with incident hypertension in early adulthood in a US nationwide cohort. Study participants were from the Growing Up Today Study (GUTS) established in 1996 (GUTSI) and 2004 (GUTSII), who were ages 9−14 (GUTSI) or 10−17 (GUTSII) at enrollment. Incident hypertension was identified by self-report on questionnaires from 2010 to 2021. We estimated residential exposures to air pollution (from spatiotemporal models), noise, and surrounding greenness throughout childhood (10-18y). We applied Cox proportional hazards models adjusted for potential confounders to assess hazard ratios (HRs) and 95% confidence intervals (CIs) associated with each interquartile range (IQR) change in exposure. We performed a quantile g-computation to assess the joint association of simultaneous exposure to the mixture. We considered potential effect modification by sex, maternal history of hypertension, overweight/obese status at age 18, urbanicity, and neighborhood socioeconomic status. Among 17,762 participants, 1530 hypertensive cases occurred during an average follow-up of 12.8 years. HRs for all exposures were small with CIs including unity. A joint HR of 1.03 (95% CI: 0.95, 1.11) was associated with a one-quartile increase across simultaneous exposure to the environmental mixture. The joint associations were stronger among non-obese participants or participants living in less advantaged neighborhoods: HRs of 1.07 (95% CI: 0.97, 1.18) and 1.08 (95% CI: 0.98, 1.18), respectively. In conclusion, we did not identify an independent or joint association between childhood exposure to air pollution, noise, and surrounding greenness and early adulthood hypertension. However, a positive joint association was suggested among non-obese participants or those living in less advantaged neighborhoods.

Ultra-processed food consumption and renal cell carcinoma incidence and mortality: results from a large prospective cohort

BackgroundGrowing evidence shows that ultra-processed food consumption is associated with the risk of cancer. However, prospective evidence is limited on renal cell carcinoma (RCC) incidence and mortality. In this study, we aimed to examine the association of ultra-processed food consumption and RCC incidence and mortality in a large cohort of US adults.MethodsA population-based cohort of 101,688 participants were included from the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. Ultra-processed food items were confirmed by using the NOVA food classification system. The consumption of ultra-processed food was expressed as a percentage of total food intake (g/day). Prospective associations were calculated using Cox regression. Restricted cubic spline regression was used to assess nonlinearity. Subgroup analyses were performed to investigate the potential effect modifiers on the incidence and mortality of RCC.ResultsA total of 410 participants developed RCC during a total of 899,731 person-years of follow-up (median 9.41 years) and 230 RCC deaths during 1,533,930 person-years of follow-up (median 16.85 years). In the fully adjusted model, participants in the highest compared with the lowest quintiles of ultra-processed food consumption had a higher risk of RCC (HR quartile 4 vs 1:1.42; 95% CI: 1.06–1.91; Ptrend = 0.004) and mortality (HR quartile 4 vs. quartile 1: 1.64; 95% CI: 1.10–2.43; Ptrend = 0.027). Linear dose–response associations with RCC incidence and mortality were observed for ultra-processed food consumption (all Pnonlinearity > 0.05). The reliability of these results was supported by sensitivity and subgroup analyses.ConclusionIn conclusion, higher consumption of ultra-processed food is associated with an increased risk of RCC incidence and mortality. Limiting ultra-processed food consumption might be a primary prevention method of RCC.

Association Between Triglyceride Glucose Index and Chronic Kidney Disease in Normal-Weight Chinese Adults With Hypertension.

This study aimed to examine the association between the triglyceride-glucose (TyG) index and chronic kidney disease (CKD) in normotensive adults with hypertension and further investigate potential effect modifiers of this association. A total of 7975 normoweight hypertensive participants were enrolled from the Chinese H-type hypertension registry (CHHRS) cohort. The TyG index was calculated using the formula: ln (fasting triglyceride [mg/dL] × fasting plasma glucose [mg/dL])/2. CKD was defined as an estimated glomerular filtration rate (eGFR) < 60mL/min/1.73 m2 of body surface area. Multivariate logistic regression analysis revealed a 50% increased risk of CKD (OR: 1.50, 95% CI: 1.26-1.79) for each unit increase in the TyG index. A linear dose-response relationship between the TyG index and CKD risk was observed using restricted cubic spline analysis. Compared to the first quartile of the TyG index, the fourth quartile showed a significantly higher risk of CKD (OR: 1.88; 95% CI: 1.41-2.50). Subgroup analysis identified a stronger association between the TyG index and CKD risk in males and individuals with a history of alcohol consumption (all p values for interaction < 0.05). In conclusions, the TyG index was significantly associated with an increased risk of CKD in normoweight adults with hypertension, particularly in males and those with a history of alcohol consumption.

Gestational exposure to organophosphate esters and autism spectrum disorder and other non-typical development in a cohort with elevated familial likelihood

BackgroundGestational exposure to organophosphate esters (OPEs) is known to affect offspring neurodevelopment in animal studies. However, epidemiological evidence is inconsistent. MethodsParticipants were 277 mother-child pairs from MARBLES (Markers of Autism Risk in Babies – Learning Early Signs), a cohort with elevated familial likelihood of autism spectrum disorder (ASD). Nine OPE biomarker concentrations were quantified in maternal urine collected during the 2nd or 3rd trimesters of pregnancy. At age 3 years, children underwent clinical assessment for ASD and were classified into ASD, other non-typical development (non-TD), or typical development (TD). Multinomial logistic regression was used to estimate associations between each OPE biomarker and relative risk ratios for ASD and non-TD compared to TD. We examined effect modification by child sex and socioeconomic status. We also conducted a secondary analysis by using a continuous measure of ASD symptom severity as an outcome. Quantile-based g-computation was performed to examine the associations for an OPE mixture. ResultsOverall, no significant association was observed between the concentrations of each OPE biomarker or their mixture and relative risk for either ASD or non-TD. Effect modifications by child sex and maternal education were not observed. When the analysis was stratified by homeownership, among non-homeowners, ASD likelihood was increased with increased levels of bis(1-chloro-2-propyl) phosphate, bis(butoxyethyl) phosphate, and sum of di-n-butyl phosphate and di-iso-butyl phosphate (DBUP/DIBP) (pint < 0.10). Higher DBUP/DIBP were associated with increased ASD symptom severity scores. ConclusionThere was no clear evidence of gestational OPE exposure in association with relative risk for ASD; however, potential effect modification by homeownership was observed. Although our cohort includes children with elevated familial likelihood of ASD, this is the first study investigating the association between gestational OPE exposure and clinically-diagnosed ASD. Further research is needed to confirm our findings in the general population.

Per- and poly-fluoroalkyl substances (PFAS) accelerate biological aging mediated by increased C-reactive protein

Unhealthy biological aging is related to higher incidence of varied age-related diseases, even higher all-cause mortality. Previous small sample size study suggested that Per- and poly-fluoroalkyl substances (PFAS) was associated with biological aging, but the evidence of exposure-response relationships, potential effect modifiers, and potential mediators were not investigated. Therefore, we conducted a cross-sectional analysis of national study including 14, 865 adults in the US from 8 survey cycles of NHANES from 2003 to 2018, to investigate the associations of PFAS compounds in body serum, including perfluorooctanoic acid (PFOA), perfluorooctane sulfonic acid (PFOS), perfluorononanoic acid (PFNA), and perfluorohexane sulfonic acid (PFHxS), with biological aging. Generalized linear models showed that higher human exposure to PFAS was associated with accelerated biological aging. Importantly, human exposure to PFOA, PFOS, PFNA, and PFHxS with detected level (above 0.10 ng/mL) was associated with an average of 3.3 year (95 %CI: 2.7, 3.9, P < 0.001), 14.9 year (95 %CI: 7.2, 22.7, P < 0.001), 10.9 years (95 %CI: 3.9, 17.7, P < 0.001), and 8.8 years (95 %CI: 4.8, 12.9, P < 0.001) of biological aging acceleration. Cubic spline models indicated exposure-response relationships where there was no safe threshold of PFAS level regarding harms to human healthy aging. The weighted sum regression model found the significant associations of PFAS compound mixture with biological aging acceleration, and PFOA was the dominant contributor among 4 PFAS compounds. Mediation analysis suggested that C-reactive protein, one of the inflammation biomarkers, might play as mediator in PFAS-induced accelerated biological aging, but not Triglyceride-glucose index. In summary, our study suggests that the effects of PFAS on biological aging acceleration should be of concern and more action plans to address their negative impact on human health should be launched.

Blast Exposure, Tinnitus, Hearing Loss, and Postdeployment Quality of Life in U.S. Veterans: A Longitudinal Analysis.

Examine the association between military blast exposure and functional status among veterans with a focus on functional disability as a proxy for quality of life and explore the potential modifying effect of hearing loss on this association. Prospective cohort. Multi-institutional tertiary referral centers. 540 veterans. Self-reported military blast exposure with and without tinnitus; high-frequency hearing loss (yes/no). WHO Disability Assessment Schedule 2.0 questionnaires at baseline and annually over 5 years. The odds of membership into three functional disability trajectory groups: low functional disability, moderate functional disability, and high functional disability. Of 540 veterans, 197 (36.5%) self-reported a blast exposure history, and 106 of 197 (53.8%) reported tinnitus as a direct result of the blast. Blast exposure without tinnitus increased the odds of moderate functional disability compared with low functional disability (odds ratio [OR] = 1.5; 95% confidence interval [CI], 0.92-2.51), which strengthened among those with blast with tinnitus (OR, 3.6; 95% CI, 2.1-6.1). Blast exposure without tinnitus also increased the odds of membership to high functional disability versus low functional disability (OR, 2.2; 95% CI, 1.1-4.8). Hearing loss further increased the odds of reporting functional disability. The probability of low functional disability was approximately 60% if there was no history of blast or hearing loss, dropping to 20% if there was blast, tinnitus, and hearing loss history. Blast exposure negatively affects the quality of life of veterans, especially when compounded with tinnitus and hearing loss.

Association between asthma and visceral adipose tissue in adults, a cross-sectional study from NHANES 2011-2018.

Asthma is a chronic inflammatory disease that affects millions of people worldwide. Obesity, particularly visceral adipose tissue (VAT), is known to secrete adipokines and pro-inflammatory factors, which are closely associated with various metabolic and cardiovascular diseases. Research indicates that these metabolic disturbances can exacerbate inflammatory conditions, contributing to both cardiovascular and respiratory diseases, including asthma. Despite these associations, studies on the specific relationship between VAT and asthma remain limited and warrant further investigation. Utilizing the NHANES database from 2011 to 2018, we included a total of 11,137 participants. Multivariable regression analysis was performed, stratifying subjects based on VAT levels and adjusting for various confounders. Subgroup interaction analysis and nonlinear analysis were conducted to explore potential effect modifiers and nonlinear associations. In this study, 11,137 participants were included, with 49.74% being female. Among the 509 asthma patients, 69.35% were female. The number of asthma patients among Non-Hispanic Whites was 212, representing 41.65% of the total, the highest proportion among the studied groups. The VAT for asthma patients was 529g, significantly higher than the 455g in the non-asthma group (P < 0.001). Multivariable regression analysis showed that for every 200g increase in VAT, the risk of asthma increased by 10.4% (P = 0.032), 20.8% (P < 0.001), and 20.3% (P = 0.004) across three models (unadjusted, adjusted for demographic factors, and fully adjusted). Subgroup analysis indicated a stronger association between VAT and asthma risk in females and individuals over 40 years old. Nonlinear analysis uncovers a J-shaped relationship between VAT and asthma, with the lowest risk observed at 464.57g (P < 0.001). The study findings suggest that increased VAT is associated with elevated asthma risk, particularly among females and older individuals. These results underscore the importance of considering VAT in asthma risk assessment and highlight potential targeted interventions to reduce asthma risk associated with excess visceral adiposity.