Faculty Bibliography
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536
Noise Exposure and Cardiovascular Health
Noise is considered an environmental stressor adversely affecting well-being and quality of life, inter-individual communications, and attention and cognitive function and inducing emotional responses, corresponding to noise annoyance. In addition, noise exposure is associated with non-auditory effects including worsening mental health, cognitive impairments, and adverse birth outcomes, sleep disorders, and increased annoyance. An accumulating body of evidence has indicated that traffic noise is also associated with CVD, through multiple pathways. It has been shown that psychological stress and mental health disorders such as depression and anxiety have a negative impact on the development of cardiovascular diseases and outcomes. Likewise, reduced sleep quality and/or duration has been reported to increase sympathetic nervous system activity, which can predispose to conditions like hypertension and diabetes mellitus, known risk factors for CVD. Finally, there seems to be a disruption in the hypothalamic-pituitary-axis secondary to noise pollution that also results in an increased risk of CVD. The World Health Organization has estimated that the number of DALYs (disability-adjusted life-years) lost resulting from environmental noise in Western Europe ranges from 1 to 1.6 million, making noise the second major contributor to the burden of disease in Europe, only after air pollution. Thus, we sought to explore the relationship between noise pollution and risk of CVD.
PMID: 37422031
ISSN: 1535-6280
CID: 5539582
Nonlinear low dose hematotoxicity of benzene; a pooled analyses of two studies among Chinese exposed workers
BACKGROUND:Impairment of the hematopoietic system is one of the primary adverse health effects from exposure to benzene. We previously have shown that exposure to benzene at low levels (<1 ppm) affects the blood forming system and that these effects were proportionally stronger at lower versus higher levels of benzene exposure. This observation is potentially explained by saturation of enzymatic systems. METHODS:Here we extend these analyses by detailed modeling of the exposure response association of benzene and its major metabolites (i.e. catechol, muconic acid, phenol, and hydroquinone) on peripheral white blood cell (WBC) counts and its major cell-subtypes (i.e. granulocytes, lymphocytes, and monocytes) using two previously published cross-sectional studies among occupationally exposed Chinese workers. RESULTS:Supra-linear exposure response associations were observed between air benzene concentrations (range ∼ 0.1 - 100 ppm) and WBC counts and its cell-subtypes, with a larger than proportional decrease in cell counts at lower than at higher levels of benzene exposure. The hematotoxicity associations were largely similar in shape when the analyses were repeated with benzene urinary metabolites suggesting that enzymatic saturation is not a full explanation of the observed non-linearity with WBC endpoints. DISCUSSION:We hypothesize that the flattening of the exposure response curve especially at higher benzene exposure levels may reflect a response by the bone marrow to maintain hematopoietic homeostasis. Toxicity to the bone marrow and an induced hyper-proliferative response could both contribute to risk of subsequently developing a hematopoietic malignancy. Additional work is needed to explore this hypothesis.
PMID: 37290291
ISSN: 1873-6750
CID: 5533562
Risk factors for head and neck cancer in more and less developed countries: Analysis from the INHANCE consortium
OBJECTIVE:We analyzed the pooled case-control data from the International Head and Neck Cancer Epidemiology (INHANCE) consortium to compare cigarette smoking and alcohol consumption risk factors for head and neck cancer between less developed and more developed countries. SUBJECTS AND METHODS/METHODS:The location of each study was categorized as either a less developed or more developed country. We compared the risk of overall head and neck cancer and cancer of specific anatomic subsites associated with cigarette smoking and alcohol consumption. Additionally, age and sex distribution between categories was compared. RESULTS:The odds ratios for head and neck cancer sites associated with smoking duration differed between less developed and more developed countries. Smoking greater than 20Â years conferred a higher risk for oral cavity and laryngeal cancer in more developed countries, whereas the risk was greater for oropharynx and hypopharynx cancer in less developed countries. Alcohol consumed for more than 20Â years conferred a higher risk for oropharynx, hypopharynx, and larynx cancer in less developed countries. The proportion of cases that were young (<45Â years) or female differed by country type for some HNC subsites. CONCLUSION/CONCLUSIONS:These findings suggest the degree of industrialization and economic development affects the relationship between smoking and alcohol with head and neck cancer.
PMID: 35322907
ISSN: 1601-0825
CID: 5200562
Sociobiome - Individual and neighborhood socioeconomic status influence the gut microbiome in a multi-ethnic population in the US
Lower socioeconomic status (SES) is related to increased incidence and mortality due to chronic diseases in adults. Association between SES variables and gut microbiome variation has been observed in adults at the population level, suggesting that biological mechanisms may underlie the SES associations; however, there is a need for larger U.S. studies that consider individual- and neighborhood-level measures of SES in racially diverse populations. In 825 participants from a multi-ethnic cohort, we investigated how SES shapes the gut microbiome. We determined the relationship of a range of several individual- and neighborhood-level SES indicators with the gut microbiome. Individual education level and occupation were self-reported by questionnaire. Geocoding was applied to link participants' addresses with neighborhood census tract socioeconomic indicators, including average income and social deprivation in the census tract. Gut microbiome was measured using 16SV4 region rRNA gene sequencing of stool samples. We compared α-diversity, β-diversity, and taxonomic and functional pathway abundance by socioeconomic status. Lower SES was significantly associated with greater α-diversity and compositional differences among groups, as measured by β-diversity. Several taxa related to low SES were identified, especially an increasing abundance of Genus Catenibacterium and Prevotella copri. The significant association between SES and gut microbiota remained even after considering the race/ethnicity in this racially diverse cohort. Together, these results showed that lower socioeconomic status was strongly associated with compositional and taxonomic measures of the gut microbiome, suggesting that SES may shape the gut microbiota.
PMID: 37131763
ISSN: 2693-5015
CID: 5738092
Validation of a Genetic-Enhanced Risk Prediction Model for Colorectal Cancer in a Large Community-Based Cohort
BACKGROUND:Polygenic risk scores (PRS) which summarize individuals' genetic risk profile may enhance targeted colorectal cancer screening. A critical step towards clinical implementation is rigorous external validations in large community-based cohorts. This study externally validated a PRS-enhanced colorectal cancer risk model comprising 140 known colorectal cancer loci to provide a comprehensive assessment on prediction performance. METHODS:The model was developed using 20,338 individuals and externally validated in a community-based cohort (n = 85,221). We validated predicted 5-year absolute colorectal cancer risk, including calibration using expected-to-observed case ratios (E/O) and calibration plots, and discriminatory accuracy using time-dependent AUC. The PRS-related improvement in AUC, sensitivity and specificity were assessed in individuals of age 45 to 74 years (screening-eligible age group) and 40 to 49 years with no endoscopy history (younger-age group). RESULTS:In European-ancestral individuals, the predicted 5-year risk calibrated well [E/O = 1.01; 95% confidence interval (CI), 0.91-1.13] and had high discriminatory accuracy (AUC = 0.73; 95% CI, 0.71-0.76). Adding the PRS to a model with age, sex, family and endoscopy history improved the 5-year AUC by 0.06 (P < 0.001) and 0.14 (P = 0.05) in the screening-eligible age and younger-age groups, respectively. Using a risk-threshold of 5-year SEER colorectal cancer incidence rate at age 50 years, adding the PRS had a similar sensitivity but improved the specificity by 11% (P < 0.001) in the screening-eligible age group. In the younger-age group it improved the sensitivity by 27% (P = 0.04) with similar specificity. CONCLUSIONS:The proposed PRS-enhanced model provides a well-calibrated 5-year colorectal cancer risk prediction and improves discriminatory accuracy in the external cohort. IMPACT:The proposed model has potential utility in risk-stratified colorectal cancer prevention.
PMCID:9992158
PMID: 36622766
ISSN: 1538-7755
CID: 5431952
Author Correction: Deciphering colorectal cancer genetics through multi-omic analysis of 100,204 cases and 154,587 controls of European and east Asian ancestries
PMID: 36782065
ISSN: 1546-1718
CID: 5427102
PM2.5 and Cardiovascular Health Risks
PM2.5 is a frequently studied particulate matter metric, due to its wide range of identified overall adverse health effects, particularly cardiovascular health risks. However, there are no clear clinical practice guidelines for air pollution in regard to the prevention of cardiovascular health risks, since most of the current medical guidelines for CVD focus on metabolic risk factors such as hyperlipidemia or diabetes. We sought to determine the relationship between PM2.5 and cardiovascular disease, cardiovascular events, and all-cause mortality by performing a systematic review and meta-analysis. We searched Ovid MEDLINE, Ovid Embase, Ovid Cochrane Database of Systematic Reviews, Scopus, and Web of Science from the database inception to December 2022 for studies that reported an association between PM2.5 and cardiovascular disease, cardiovascular events, and all-cause mortality. We used the DerSimonian & Laird random-effects method to pool hazard ratios or risk ratios separately from the included studies. Of the total 18 prospective studies, 7,300,591 individuals were followed for a median follow-up of 9 years. Compared to low long-term exposure to PM 2.5 levels, an increase in exposure to PM 2.5 levels resulted in an increase in all-cause mortality (HR 1.08 95% CI of 1.05-1.11, P < 0.05). Similarly, when compared to a low long-term exposure to PM 2.5 levels, an increase in exposure to PM 2.5 levels resulted in an increase in cardiovascular disease (HR 1.09, 95% CI of 1.00-1.18, P < 0.05) and an increase in cardiovascular disease mortality (HR 1.12, 95% CI of 1.07-1.18, P < 0.05). Increased exposure to PM 2.5 levels is significantly associated with an increased risk of all-cause mortality, cardiovascular disease, and cardiovascular disease mortality. Although federal primary and secondary standards are in place, those standards are not low enough to prevent CVD health effects. Clinicians should emphasize PM2.5 as a modifiable CV risk factors for their patients to potentially reduce the development of CV complications. A clinical action guideline is needed specifically for air pollution effects on CVD, and how to mitigate them.
PMID: 36828043
ISSN: 1535-6280
CID: 5434092
Grain, Gluten, and Dietary Fiber Intake Influence Gut Microbial Diversity: Data from the Food and Microbiome Longitudinal Investigation
UNLABELLED:< 0.05). These findings suggest that whole grain and dietary fiber are associated with overall gut microbiome structure, largely fiber-fermenting microbiota. Higher refined grain and gluten intakes may be associated with lower microbial diversity. SIGNIFICANCE:Regular consumption of whole grains and dietary fiber was associated with greater abundance of gut bacteria that may lower risk of colorectal cancer. Further research on the association of refined grains and gluten with gut microbial composition is needed to understand their roles in health and disease.
PMCID:10035461
PMID: 36968219
ISSN: 2767-9764
CID: 5594522
Deciphering colorectal cancer genetics through multi-omic analysis of 100,204 cases and 154,587 controls of European and east Asian ancestries
Colorectal cancer (CRC) is a leading cause of mortality worldwide. We conducted a genome-wide association study meta-analysis of 100,204 CRC cases and 154,587 controls of European and east Asian ancestry, identifying 205 independent risk associations, of which 50 were unreported. We performed integrative genomic, transcriptomic and methylomic analyses across large bowel mucosa and other tissues. Transcriptome- and methylome-wide association studies revealed an additional 53 risk associations. We identified 155 high-confidence effector genes functionally linked to CRC risk, many of which had no previously established role in CRC. These have multiple different functions and specifically indicate that variation in normal colorectal homeostasis, proliferation, cell adhesion, migration, immunity and microbial interactions determines CRC risk. Crosstissue analyses indicated that over a third of effector genes most probably act outside the colonic mucosa. Our findings provide insights into colorectal oncogenesis and highlight potential targets across tissues for new CRC treatment and chemoprevention strategies.
PMID: 36539618
ISSN: 1546-1718
CID: 5394972
Elevated dietary carbohydrate and glycemic intake associate with an altered oral microbial ecosystem in two large U.S. cohorts
The human oral microbiome is associated with chronic diseases including cancer. However, our understanding of its relationship with diet is limited. We assessed the associations between carbohydrate and glycemic index (GI) with oral microbiome composition in 834 non-diabetic subjects from the NCI-PLCO and ACS-CPSII cohorts. The oral microbiome was characterized using 16Sv3-4 rRNA-sequencing from oral mouthwash samples. Daily carbohydrate and GI were assessed from food frequency questionnaires. We used linear regression, permutational MANOVA, and negative binomial Generalized Linear Models (GLM) to test associations of diet with α- and β-diversity and taxon abundance (adjusting for age, sex, cohort, BMI, smoking, caloric intake, and alcohol). A q-value (FDR-adjusted P-value) of <0.05 was considered significant. Oral bacterial α-diversity trended higher in participants in the highest quintiles of carbohydrate intake, with marginally increased richness and Shannon diversity (p-trend=0.06 and 0.07). Greater carbohydrate intake was associated with greater abundance of class Fusobacteriia (q=0.02) and genus Leptotrichia (q=0.01) and with lesser abundance of an Actinomyces OTU (q=4.7E-04). Higher GI was significantly related to greater abundance of genus Gemella (q=0.001). This large, nationwide study provides evidence that diets high in carbohydrates and GI may influence the oral microbiome.
PMCID:9770587
PMID: 36567732
ISSN: 2767-9764
CID: 5592052
