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Background Concurrent use of marijuana and alcohol in drivers is of increasing concern but its role in crash causation has not been well understood. Methods Using a case–control design, we assessed the individual and joint effects of marijuana and alcohol use on fatal crash risk. Cases ( n  = 1944) were drivers fatally injured in motor vehicle crashes in the United States at specific times in 2006, 2007 and 2008. Controls ( n  = 7719) were drivers who participated in the 2007 National Roadside Survey of Alcohol and Drug Use by Drivers. Results Overall, cases were significantly more likely than controls to test positive for marijuana (12.2% vs. 5.9%, p  < 0.0001), alcohol (57.8% vs. 7.7%, p  < 0.0001) and both marijuana and alcohol (8.9% vs. 0.8%, p  < 0.0001). Compared to drivers testing negative for alcohol and marijuana, the adjusted odds ratios of fatal crash involvement were 16.33 [95% confidence interval (CI): 14.23, 18.75] for those testing positive for alcohol and negative for marijuana, 1.54 (95% CI: 1.16, 2.03) for those testing positive for marijuana and negative for alcohol, and 25.09 (95% CI: 17.97, 35.03) for those testing positive for both alcohol and marijuana. Conclusions Alcohol use and marijuana use are each associated with significantly increased risks of fatal crash involvement. When alcohol and marijuana are used together, there exists a positive synergistic effect on fatal crash risk on the additive scale.

A growing body of evidence supports an antiobesity effect of dairy products; however, the mechanisms remain unclear. The objective of this study was to explore possible intestinal mechanisms by which dairy delivers an antiobesity effect. The human intestinal cell line, NCI-H716, was used to test the hypothesis that branched-chain amino acids and dairy proteins regulate satiety hormone secretion and modulate genes involved in fatty acid and cholesterol metabolism. In dose–response (0.5%, 1.0%, 2.0%, and 3.0%) studies, the effect of leucine, isoleucine, valine, skim milk, casein, and whey on glucagon-like peptide-1 release and the expression of selected genes were tested. Leucine, isoleucine, skim milk, and casein stimulated glucagon-like peptide-1 release ( P < 0.05). Isoleucine and whey downregulated the expression of intestinal-type fatty acid binding protein ( i-FABP), fatty acid transport protein 4 ( FATP4), Niemann-Pick C-1–like-1 protein ( NPC1L1), acetyl-coenzyme A carboxylase ( ACC), fatty acid synthase ( FAS), sterol regulatory element-binding protein-2 ( SREBP-2), and 3-hydroxy-3-methylglutaryl-CoA reductase ( HMGCR; P < 0.05). Leucine and valine downregulated the expression of NPC1L1, ACC, FAS, SREBP-2, and HMGCR ( P < 0.05). Casein downregulated the expression of i-FABP, FATP4, ACC, FAS, SREBP-2, and HMGCR ( P < 0.05). Skim milk downregulated the expression of ACC, FAS, and SREBP-2, but not i-FABP, FATP4, and NPC1L1. This work suggests that the antiobesity effect of dairy may be mediated, at least in part, by integration of events that promote glucagon-like peptide-1 secretion and inhibit expression of genes involved in intestinal fatty acid and cholesterol absorption and synthesis.

BackgroundCannabis use has been causally linked to violent behaviors in experimental and case studies, but its association with homicide victimization has not been rigorously assessed through epidemiologic research.MethodsWe performed a case-control analysis using two national data systems. Cases were homicide victims from the National Violent Death Reporting System (NVDRS), and controls were participants from the National Survey on Drug Use and Health (NSDUH). While the NVDRS contained toxicological testing data on cannabis use, the NSDUH only collected self-reported data, and thus the potential misclassification in the self-reported data needed to be corrected. We took a data fusion approach by concatenating the NSDUH with a third data system, the National Roadside Survey of Alcohol and Drug Use by Drivers (NRS), which collected toxicological testing and self-reported data on cannabis use for drivers. The data fusion approach provided multiple imputations (MIs) of toxicological testing results on cannabis use for the participants in the NSDUH, which were then used in the case-control analysis. Bootstrap was used to obtain valid statistical inference.ResultsThe analyses revealed that cannabis use was associated with 3.55-fold (95% CI: 2.75–4.35) increased odds of homicide victimization. Alcohol use, being Black, male, aged 21–34 years, and having less than a high school education were also significantly associated with increased odds of homicide victimization.ConclusionsCannabis use is a major risk factor for homicide victimization. The data fusion with MI method is useful in integrative data analysis for harmonizing measures between different data sources.

Objectives. We explore how misclassification in disease status can distort the exposure–disease association in a study with dichotomous disease and exposure status. Methods. We define the difference in population odds ratios between populations with and without disease misclassification as population-level bias and derive the bias as a function of sensitivity and specificity for observed disease status. The magnitude and direction of bias can be elucidated through analytic derivations, as illustrated with numerical examples. Results. Patterns of bias exist not only for nondifferential misclassification but also for some differential misclassification scenarios. We have provided conditions defined in terms of sensitivity and specificity that correspond to each pattern of bias. Conclusions. Caution is needed in interpreting results when misclassification is present. Our findings can be used to assess the effects of disease misclassification in a population when sensitivity and specificity are known or can be estimated.

BackgroundOverdose mortality increased substantially during the COVID-19 pandemic, but it is unclear to what extent the COVID-19 mortality had contributed to this increase at the neighborhood level.MethodsThis was an ecological study based on New York City United Hospital Fund (NYC UHF) neighborhood-level data from 2019 to 2021, split into two time-windows: pre-COVID (2019) and during-COVID (2020 and 2021). Linear regression models were used to estimate the effect of cumulative COVID-19 mortality on the increase in drug overdose mortality from the pre-COVD to during-COVID periods at the neighborhood level, with and without adjusting for neighborhood characteristics.ResultsDrug overdose mortality rate increased from 21.3 to 33.4 deaths per 100,000 person-years across NYC UHF neighborhoods from pre-COVID to during-COVID. For each additional COVID-19 death per 1,000 person-years at the neighborhood level, the increase in drug overdose mortality rose 2.4 (95% CI: 1.7, 3.3) times. Furthermore, neighborhoods with a higher percentage of Hispanic residents, a higher percentage of single-person households, and a higher percentage of residents with health insurance experienced significantly larger increases in drug overdose mortality. In contrast, neighborhoods with a higher percentage of residents aged 75 and older had a smaller increase in drug overdose mortality.ConclusionsNYC neighborhoods with higher cumulative COVID-19 mortality experienced a greater increase in drug overdose mortality during the first two years of the COVID-19 pandemic.

Objectives: To examine the longitudinal association between subclinical hearing loss (SCHL) and neurocognitive performance Design: Longitudinal analyses were conducted among 2,115 subjects who underwent audiometric testing in a US multi-centered epidemiologic cohort study. The primary exposure was better ear hearing (pure tone average). SCHL was defined as hearing ≤25 dB. The primary outcome was neurocognitive performance, measured by Digit Symbol Substitution Test (DSST), Modified Mini Mental State Examination (3MS), and CLOX1. Linear mixed models were performed to assess the longitudinal association between hearing and cognitive performance, adjusting for covariates. Models were fit among all individuals and among individuals with SCHL only. Results: Among 2,115 participants, mean (SD) age was 73.5 (2.9) years; 52.3% were women. Mean (SD) better ear pure tone average was 30.0 (13.1) dB. Mean follow-up was 9.1 years (range 3-16). Among all participants, worse hearing was associated with significantly steeper cognitive decline measured by the DSST (0.054-point/year steeper decrease per 10 dB worse hearing, 95% confidence interval [CI]: 0.026-0.082) and 3MS (0.043-point/year steeper decrease per 10 dB worse hearing, CI: 0.025-0.062), but not CLOX1. Among those with SCHL, worse hearing was associated with significantly steeper cognitive performance decline as measured by DSST (0.121-point/year steeper decrease per 10 dB worse hearing, CI: 0.013-0.228), but not CLOX1 or 3MS. Conclusions: Among those with SCHL, worse hearing was associated with steeper cognitive performance declines over time as measured by DSST. The relationship between hearing loss and cognition may begin at earlier levels of hearing loss than previously recognized.

Background: Recent cross-sectional studies suggest a link between butylbenzyl phthalate (BBzP) in house dust and childhood eczema. Objectives: We aimed to evaluate whether concentrations of monobenzyl phthalate (MBzP), the main BBzP metabolite in urine, during pregnancy are associated prospectively with eczema in young children, and whether this association varies by the child's sensitization to indoor allergens or serological evidence of any allergies. Methods: MBzP was measured in spot urine samples during the third trimester of pregnancy from 407 African-American and Dominican women residing in New York City in 1999—2006. Repeated questionnaires asked mothers whether their doctor ever said their child had eczema. Child blood samples at 24, 36, and 60 months of age were analyzed for total, anti-cockroach, dust mite, and mouse IgE. Relative risks (RR) were estimated with multivariable modified Poisson regression. Analyses included a multinomial logistic regression model for early- and late-onset eczema versus no eczema through 60 months of age. Results: MBzP was detected in > 99% of samples (geometric mean = 13.6; interquartile range: 5.7—31.1 ng/mL). By 24 months, 30% of children developed eczema, with the proportion higher among African Americans (48%) than among Dominicans (21%) (p < 0.001). An interquartile range increase in log MBzP concentration was associated positively with early-onset eczema (RR = 1.52 for eczema by 24 months; 95% confidence interval: 1.21, 1.91, p = 0.0003, n = 113 reporting eczema/376 total sample), adjusting for urine specific gravity, sex, and race/ethnicity. MBzP was not associated with allergic sensitization, nor did seroatopy modify consistently the MBzP and eczema association. Conclusions: Prenatal exposure to BBzP may influence the risk of developing eczema in early childhood.

Background While laboratory testing for infectious diseases such as COVID-19 is the surveillance gold standard, it is not always feasible, particularly in settings where resources are scarce. In the small country of Lesotho, located in sub-Saharan Africa, COVID-19 testing has been limited, thus surveillance data available to local authorities are limited. The goal of this study was to compare a participatory influenza-like illness (ILI) surveillance system in Lesotho with COVID-19 case count data, and ultimately to determine whether the participatory surveillance system adequately estimates the case count data. Methods A nationally-representative sample was called on their mobile phones weekly to create an estimate of incidence of ILI between July 2020 and July 2021. Case counts from the website Our World in Data (OWID) were used as the gold standard to which our participatory surveillance data were compared. We calculated Spearman’s and Pearson’s correlation coefficients to compare the weekly incidence of ILI reports to COVID-19 case count data. Results Over course of the study period, an ILI symptom was reported 1,085 times via participatory surveillance for an average annual cumulative incidence of 45.7 per 100 people (95% Confidence Interval [CI]: 40.7 – 51.4). The cumulative incidence of reports of ILI symptoms was similar among males (46.5, 95% CI: 39.6 – 54.4) and females (45.1, 95% CI: 39.8 – 51.1). There was a slightly higher annual cumulative incidence of ILI among persons living in peri-urban (49.5, 95% CI: 31.7 – 77.3) and urban settings compared to rural areas. The January peak of the participatory surveillance system ILI estimates correlated significantly with the January peak of the COVID-19 case count data (Spearman’s correlation coefficient = 0.49; P  < 0.001) (Pearson’s correlation coefficient = 0.67; P  < 0.0001). Conclusions The ILI trends captured by the participatory surveillance system in Lesotho mirrored trends of the COVID-19 case count data from Our World in Data. Public health practitioners in geographies that lack the resources to conduct direct surveillance of infectious diseases may be able to use cell phone-based data collection to monitor trends.

Experimental and/or epidemiological studies suggest that prenatal exposure to bisphenol A (BPA) may delay fetal lung development and maturation and increase the susceptibility to childhood respiratory disease. However, the underlying mechanisms remain to be elucidated. In our previous study with cultured human fetal lung fibroblasts (HFLF), we demonstrated that 24-h exposure to 1 and 100 µM BPA increased GPR30 protein in the nuclear fraction. Exposure to 100 μM BPA had no effects on cell viability, but increased cytoplasmic expression of ERβ and release of GDF-15, as well as decreased release of IL-6, ET-1, and IP-10 through suppression of NFκB phosphorylation. By performing global gene expression and pathway analysis in this study, we identified molecular pathways, gene networks, and key molecules that were affected by 100, but not 0.01 and 1 µM BPA in HFLF. Using multiple genomic and proteomic tools, we confirmed these changes at both gene and protein levels. Our data suggest that 100 μM BPA increased CYP1B1 and HSD17B14 gene and protein expression and release of endogenous estradiol, which was associated with increased ROS production and DNA double-strand breaks, upregulation of genes and/or proteins in steroid synthesis and metabolism, and activation of Nrf2-regulated stress response pathways. In addition, BPA activated ATM-p53 signaling pathway, resulting in increased cell cycle arrest at G1 phase, senescence and autophagy, and decreased cell proliferation in HFLF. The results suggest that prenatal exposure to BPA at certain concentrations may affect fetal lung development and maturation, and thereby affecting susceptibility to childhood respiratory diseases.