Environmental Epidemiology最新文献

{"title":"Exposure to ambient polycyclic aromatic hydrocarbons and early-onset female breast cancer in a case-control study in Ontario, Canada.","authors":"Claudia M Waddingham, Patrick Hinton, Paul J Villeneuve, Jeffrey R Brook, Eric Lavigne, Kristian Larsen, Will D King, Deyong Wen, Jun Meng, Junhua Zhang, Elisabeth Galarneau, Shelley A Harris","doi":"10.1097/EE9.0000000000000333","DOIUrl":"10.1097/EE9.0000000000000333","url":null,"abstract":"<p><strong>Background: </strong>Ambient polycyclic aromatic hydrocarbons (PAHs) are a class of toxicologically important and understudied air pollutants. Epidemiologic evidence suggests that chronic exposure to PAHs increases breast cancer risk; however, there are few studies in nonoccupational settings that focus on early-onset diagnoses.</p><p><strong>Methods: </strong>The relationship between residentially-based ambient PAH concentrations and female breast cancer, among those 18-45 years of age, was characterized in the Ontario Environment and Health Study (OEHS). The OEHS was a population-based case-control study undertaken in Ontario, Canada between 2013 and 2015. Primary incident breast cancers were identified within 3 months of diagnosis, and a population-based series of controls were recruited. Concentrations of ambient PAHs, using fluoranthene as a surrogate, were derived using a chemical transport model at a 2.5 km spatial resolution. These estimates were assigned to participants' residences at the time of the interview and 5 years prior. Logistic regression was used to estimate odds ratios (ORs) and their 95% confidence intervals (CIs) based on a quartile categorization of fluoranthene exposure while adjusting for a series of individual- and area-level risk factors. The shape of the exposure-response trend was evaluated using cubic splines.</p><p><strong>Results: </strong>Median fluoranthene exposure for cases and controls was 0.0017 µg/m³ and 0.0014 µg/m³, respectively. In models adjusted for a parsimonious set of risk factors, the highest quartile of exposure was associated with an increased risk of breast cancer (OR = 2.16; 95% CI = 1.22, 3.84). Restricted spline analyses revealed nonlinear dose-response patterns.</p><p><strong>Conclusions: </strong>These findings support the hypothesis that ambient PAH exposures increases the risk of early-onset breast cancer.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11463212/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142389006","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Road-traffic noise exposure and coronary atherosclerosis in the Swedish CArdioPulmonary bioImage Study (SCAPIS).","authors":"Marat Murzabekov, Åsa Persson, Christian Asker, Karl Kilbo Edlund, Charlotta Eriksson, Tomas Jernberg, Peter Molnar, Anna Oudin, Andrei Pyko, Jenny Lindvall, Mare Lõhmus, Kerstin Persson Waye, Johan Nilsson Sommar, Leo Stockfelt, Mårten Spanne, Magnus Svartengren, Mikael Ögren, Göran Pershagen, Petter Ljungman","doi":"10.1097/EE9.0000000000000344","DOIUrl":"10.1097/EE9.0000000000000344","url":null,"abstract":"<p><strong>Background: </strong>Road-traffic noise may influence the development of cardiovascular events such as stroke and myocardial infarction, but etiological mechanisms remain unclear. This study aimed to assess the relationship between long-term road-traffic noise exposure and coronary atherosclerosis in Sweden.</p><p><strong>Methods: </strong>In the Swedish CArdioPulmonary bioImage Study (SCAPIS) cohort, including 30,154 subjects aged 50-65 years, recruited between 2013 and 2018, coronary atherosclerosis was measured based on computer tomography (CT) scans as coronary artery calcium score, segment involvement score (SIS), and non-calcified plaques (NCP) at enrollment. Based on modified Nordic model, road-traffic noise exposure was modeled for 2000, 2013, and 2018 with interpolation for intermediate years. We investigated the association between time-weighted long-term exposure to road-traffic noise (L_den) and the prevalence of atherosclerosis using ordinal logistic regression models adjusting for potential socioeconomic, behavioral, and environmental confounders, including air pollution.</p><p><strong>Results: </strong>No clear associations were found between road-traffic noise and coronary atherosclerosis. The odds ratio for coronary artery calcium score was 1.00 (95% confidence interval [CI] = 0.96, 1.04), SIS 0.99 (0.96, 1.03), and NCP 0.98 (0.90, 1.03) per interquartile range (9.4 dB L_den) for road-traffic noise exposure during 10 years before enrollment. No consistent associations were observed in site-specific analyses or using shorter exposure periods. Furthermore, exposure-response analyses revealed no clear trends, and there were no strong interactions between road-traffic noise and cardiovascular risk factors in relation to the atherosclerosis markers.</p><p><strong>Conclusions: </strong>Long-term exposure to road-traffic noise was not linked to coronary atherosclerosis or calcification in relatively healthy, middle-aged populations in Sweden.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11452091/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142380305","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Temperature-mortality associations by age and cause: a multi-country multi-city study.","authors":"Noah Scovronick, Francesco Sera, Bryan Vu, Ana M Vicedo-Cabrera, Dominic Roye, Aurelio Tobias, Xerxes Seposo, Bertil Forsberg, Yuming Guo, Shanshan Li, Yasushi Honda, Rosana Abrutzky, Micheline de Sousa Zanotti Stagliorio Coelho, Paulo H Nascimento Saldiva, Eric Lavigne, Haidong Kan, Samuel Osorio, Jan Kyselý, Aleš Urban, Hans Orru, Ene Indermitte, Jouni J Jaakkola, Niilo Ryti, Mathilde Pascal, Klea Katsouyanni, Fatemeh Mayvaneh, Alireza Entezari, Patrick Goodman, Ariana Zeka, Paola Michelozzi, Francesca de'Donato, Masahiro Hashizume, Barak Alahmad, Antonella Zanobetti, Joel Schwartz, Miguel Hurtado Diaz, C De La Cruz Valencia, Shilpa Rao, Joana Madureira, Fiorella Acquaotta, Ho Kim, Whanhee Lee, Carmen Iniguez, Martina S Ragettli, Yue L Guo, Tran Ngoc Dang, Do V Dung, Benedict Armstrong, Antonio Gasparrini","doi":"10.1097/EE9.0000000000000336","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000336","url":null,"abstract":"<p><strong>Background: </strong>Heterogeneity in temperature-mortality relationships across locations may partly result from differences in the demographic structure of populations and their cause-specific vulnerabilities. Here we conduct the largest epidemiological study to date on the association between ambient temperature and mortality by age and cause using data from 532 cities in 33 countries.</p><p><strong>Methods: </strong>We collected daily temperature and mortality data from each country. Mortality data was provided as daily death counts within age groups from all, cardiovascular, respiratory, or noncardiorespiratory causes. We first fit quasi-Poisson regression models to estimate location-specific associations for each age-by-cause group. For each cause, we then pooled location-specific results in a dose-response multivariate meta-regression model that enabled us to estimate overall temperature-mortality curves at any age. The age analysis was limited to adults.</p><p><strong>Results: </strong>We observed high temperature effects on mortality from both cardiovascular and respiratory causes compared to noncardiorespiratory causes, with the highest cold-related risks from cardiovascular causes and the highest heat-related risks from respiratory causes. Risks generally increased with age, a pattern most consistent for cold and for nonrespiratory causes. For every cause group, risks at both temperature extremes were strongest at the oldest age (age 85 years). Excess mortality fractions were highest for cold at the oldest ages.</p><p><strong>Conclusions: </strong>There is a differential pattern of risk associated with heat and cold by cause and age; cardiorespiratory causes show stronger effects than noncardiorespiratory causes, and older adults have higher risks than younger adults.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11424137/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142343928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Relationship between short-term exposure to sulfur dioxide and emergency ambulance dispatches due to cardiovascular disease.","authors":"Xuerui Bai, Hongying Qu, Zebing Ye, Ruoting Wang, Guanhao He, Zhongguo Huang, Zhiying Jiang, Changfa Zhang, Shuai Li, Guowei Li","doi":"10.1097/EE9.0000000000000341","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000341","url":null,"abstract":"<p><strong>Background: </strong>The relationship between sulfur dioxide (SO₂) and cardiovascular disease (CVD) remains inconclusive. We aimed to clarify the association between short-term exposure to SO₂ and emergency ambulance dispatches (EADs) due to CVD.</p><p><strong>Methods: </strong>We collected daily data on the number of EADs due to CVD, air pollutants, and meteorological factors between October 2013 and June 2018 in Guangzhou, China. We used the quasi-Poisson generalized additive model combined with a distributed lag nonlinear model to estimate the short-term effect of SO₂ on EADs due to CVD in multivariable models. Subgroup and sensitivity analyses were also performed.</p><p><strong>Results: </strong>A total of 37,889 EADs due to CVD were documented during the study period. The average daily SO₂ concentration was 12.5 μg/m³. A significant relationship between SO₂ and EADs due to CVD was found, with a relative risk of 1.04 (95% confidence interval: 1.02, 1.06) with each 10 μg/m³ increment of SO₂ at lag 0-1_. The relationship was stronger in males, for participants aged ≥65 years, and in the cold season; however, no significant modification by subgroup was found in the association between SO₂ and EADs due to CVD. Similar results from sensitivity analyses to the main findings were observed.</p><p><strong>Conclusions: </strong>Short-term exposure to SO₂ was significantly associated with increased EADs due to CVD.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11424135/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142343927","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between phthalate exposure and sleep quality in pregnant women: Results from the Korean Children's Environmental Health Study with repeated assessment of exposure.","authors":"Dirga Kumar Lamichhane, Eunhee Ha, Amanda V Bakian, Yun-Chul Hong, Dong-Wook Lee, Myung-Sook Park, Sanghwan Song, Suejin Kim, Hyunju Park, Woo Jin Kim, Jisuk Bae, Hwan-Cheol Kim","doi":"10.1097/EE9.0000000000000329","DOIUrl":"10.1097/EE9.0000000000000329","url":null,"abstract":"<p><strong>Background: </strong>Evidence linking environmental toxicants to sleep quality is growing; however, these associations during pregnancy remain unclear. We examined the associations of repeated measures of urinary phthalates in early and late pregnancy with multiple markers of sleep quality among pregnant women.</p><p><strong>Methods: </strong>The study population included 2324 pregnant women from the Korean Children's Environmental Health Study. We analyzed spot urine samples collected at two time points during pregnancy for exposure biomarkers of eight phthalate metabolites. We investigated associations between four summary phthalates (all phthalates: ∑Phthalates; di-(2-ethylhexyl) phthalate: ∑DEHP; phthalates from plastic sources: ∑Plastic; and antiandrogenic phthalates: ∑AA) and eight individual phthalates and self-reported sleep measures using generalized ordinal logistic regression and generalized estimating equations models that accounted for repeated exposure measurements. The models were adjusted for age, body mass index, education, gestational age, income, physical activity, smoking, occupation, chronic diseases, depression, and urinary cotinine levels.</p><p><strong>Results: </strong>Multiple individual phthalates and summary measures of phthalate mixtures, including ∑Plastic, ∑DEHP, ∑AA, and ∑Phthalates, were associated with lower sleep efficiency. To illustrate, every 1-unit log increase in ∑AA was associated with a reduction of sleep efficiency by 1.37 % (95% confidence interval [CI] = -2.41, -0.32). ∑AA and ∑Phthalates were also associated with shorter sleep duration and longer sleep latency. Associations between summary phthalate measures and sleep efficiency differed by urinary cotinine levels (<i>P</i> for subgroup difference < 0.05).</p><p><strong>Conclusions: </strong>Findings suggest that higher phthalate exposure may be related to lower sleep efficiency, shorter sleep duration, and prolonged sleep latency during pregnancy.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11338265/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142016766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Simulating the impact of greenspace exposure on metabolic biomarkers in a diverse population living in San Diego, California: A g-computation application.","authors":"Anaïs Teyton, Nivedita Nukavarapu, Noémie Letellier, Dorothy D Sears, Jiue-An Yang, Marta M Jankowska, Tarik Benmarhnia","doi":"10.1097/EE9.0000000000000326","DOIUrl":"10.1097/EE9.0000000000000326","url":null,"abstract":"<p><strong>Introduction: </strong>Growing evidence exists that greenspace exposure can reduce metabolic syndrome risk, a growing public health concern with well-documented inequities across population subgroups. We capitalize on the use of g-computation to simulate the influence of multiple possible interventions on residential greenspace on nine metabolic biomarkers and metabolic syndrome in adults (N = 555) from the 2014-2017 Community of Mine Study living in San Diego County, California.</p><p><strong>Methods: </strong>Normalized difference vegetation index (NDVI) exposure from 2017 was averaged across a 400-m buffer around the participants' residential addresses. Participants' fasting plasma glucose, total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and triglyceride concentrations, systolic and diastolic blood pressure, hemoglobin A1c (%), waist circumference, and metabolic syndrome were assessed as outcomes of interest. Using parametric g-computation, we calculated risk differences for participants being exposed to each decile of the participant NDVI distribution compared to minimum NDVI. Differential health impacts from NDVI exposure by sex, ethnicity, income, and age were examined.</p><p><strong>Results: </strong>We found that a hypothetical increase in NDVI exposure led to a decrease in hemoglobin A1c (%), glucose, and high-density lipoprotein cholesterol concentrations, an increase in fasting total cholesterol, low-density lipoprotein cholesterol, and triglyceride concentrations, and minimal changes to systolic and diastolic blood pressure, waist circumference, and metabolic syndrome. The impact of NDVI changes was greater in women, Hispanic individuals, and those under 65 years old.</p><p><strong>Conclusions: </strong>G-computation helps to simulate the potential health benefits of differential NDVI exposure and identifies which subpopulations can benefit most from targeted interventions aimed at minimizing health disparities.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11309718/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141906241","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reviewing umbrella reviews of systematic reviews of original studies on the effects of air pollution on disease.","authors":"Bert Brunekreef, Kurt Straif, Neil Pearce","doi":"10.1097/EE9.0000000000000324","DOIUrl":"10.1097/EE9.0000000000000324","url":null,"abstract":"","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11305730/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141901338","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Choices of morbidity outcomes and concentration-response functions for health risk assessment of long-term exposure to air pollution.","authors":"Francesco Forastiere, Joseph V Spadaro, Carla Ancona, Zorana Jovanovic Andersen, Ilaria Cozzi, Sophie Gumy, Dejan Loncar, Pierpaolo Mudu, Sylvia Medina, Roman Perez Velasco, Heather Walton, Jiawei Zhang, Michal Krzyzanowski","doi":"10.1097/EE9.0000000000000314","DOIUrl":"10.1097/EE9.0000000000000314","url":null,"abstract":"<p><strong>Background: </strong>Air pollution health risk assessment (HRA) has been typically conducted for all causes and cause-specific mortality based on concentration-response functions (CRFs) from meta-analyses that synthesize the evidence on air pollution health effects. There is a need for a similar systematic approach for HRA for morbidity outcomes, which have often been omitted from HRA of air pollution, thus underestimating the full air pollution burden. We aimed to compile from the existing systematic reviews and meta-analyses CRFs for the incidence of several diseases that could be applied in HRA. To achieve this goal, we have developed a comprehensive strategy for the appraisal of the systematic reviews and meta-analyses that examine the relationship between long-term exposure to particulate matter with an aerodynamic diameter smaller than 2.5 µm (PM_2.5), nitrogen dioxide (NO₂), or ozone (O₃) and incidence of various diseases.</p><p><strong>Methods: </strong>To establish the basis for our evaluation, we considered the causality determinations provided by the US Environmental Protection Agency Integrated Science Assessment for PM_2.5, NO₂, and O₃. We developed a list of pollutant/outcome pairs based on these assessments and the evidence of a causal relationship between air pollutants and specific health outcomes. We conducted a comprehensive literature search using two databases and identified 75 relevant systematic reviews and meta-analyses for PM_2.5 and NO₂. We found no relevant reviews for long-term exposure to ozone. We evaluated the reliability of these studies using an adaptation of the AMSTAR 2 tool, which assesses various characteristics of the reviews, such as literature search, data extraction, statistical analysis, and bias evaluation. The tool's adaptation focused on issues relevant to studies on the health effects of air pollution. Based on our assessment, we selected reviews that could be credible sources of CRF for HRA. We also assessed the confidence in the findings of the selected systematic reviews and meta-analyses as the sources of CRF for HRA. We developed specific criteria for the evaluation, considering factors such as the number of included studies, their geographical distribution, heterogeneity of study results, the statistical significance and precision of the pooled risk estimate in the meta-analysis, and consistency with more recent studies. Based on our assessment, we classified the outcomes into three lists: list A (a reliable quantification of health effects is possible in an HRA), list B+ (HRA is possible, but there is greater uncertainty around the reliability of the CRF compared to those included on list A), and list B- (HRA is not recommended because of the substantial uncertainty of the CRF).</p><p><strong>Results: </strong>In our final evaluation, list A includes six CRFs for PM_2.5 (asthma in children,","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11265782/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141751404","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genome-wide DNA methylation profiles and breast cancer among World Trade Center survivors.","authors":"Stephanie Tuminello, Yibeltal Arega Ashebir, Chanel Schroff, Sitharam Ramaswami, Nedim Durmus, Yu Chen, Matija Snuderl, Yongzhao Shao, Joan Reibman, Alan A Arslan","doi":"10.1097/EE9.0000000000000313","DOIUrl":"10.1097/EE9.0000000000000313","url":null,"abstract":"<p><strong>Background: </strong>Increased incidence of cancer has been reported among World Trade Center (WTC)-exposed persons. Aberrant DNA methylation is a hallmark of cancer development. To date, only a few small studies have investigated the relationship between WTC exposure and DNA methylation. The main objective of this study was to assess the DNA methylation profiles of WTC-exposed community members who remained cancer free and those who developed breast cancer.</p><p><strong>Methods: </strong>WTC-exposed women were selected from the WTC Environmental Health Center clinic, with peripheral blood collected during routine clinical monitoring visits. The reference group was selected from the NYU Women's Health Study, a prospective cohort study with blood samples collected before 9 November 2001. The Infinium MethylationEPIC array was used for global DNA methylation profiling, with adjustments for cell type composition and other confounders. Annotated probes were used for biological pathway and network analysis.</p><p><strong>Results: </strong>A total of 64 WTC-exposed (32 cancer free and 32 with breast cancer) and 32 WTC-unexposed (16 cancer free and 16 with prediagnostic breast cancer) participants were included. Hypermethylated cytosine-phosphate-guanine probe sites (defined as <i>β</i> > 0.8) were more common among WTC-exposed versus unexposed participants (14.3% vs. 4.5%, respectively, among the top 5000 cytosine-phosphate-guanine sites). Cancer-related pathways (e.g., human papillomavirus infection, cGMP-PKG) were overrepresented in WTC-exposed groups (breast cancer patients and cancer-free subjects). Compared to the unexposed breast cancer patients, 47 epigenetically dysregulated genes were identified among WTC-exposed breast cancers. These genes formed a network, including Wnt/β-catenin signaling genes <i>WNT4</i> and <i>TCF7L2</i>, and dysregulation of these genes contributes to cancer immune evasion.</p><p><strong>Conclusion: </strong>WTC exposure likely impacts DNA methylation and may predispose exposed individuals toward cancer development, possibly through an immune-mediated mechanism.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11152787/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141260394","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations between use of chemical hair products and epigenetic age: Findings from the Sister Study","authors":"Che-Jung Chang, Katie M. O’Brien, J. Kresovich, J. Nwanaji-Enwerem, Zongli Xu, S. Gaston, Chandra L. Jackson, Dale P. Sandler, Jack A. Taylor, Alexandra J White","doi":"10.1097/EE9.0000000000000311","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000311","url":null,"abstract":"Background: Hair products may be a source of harmful chemicals and have been linked to age-related health outcomes. We investigated whether the use of hair products is related to epigenetic age in a sample of Black (both Hispanic and non-Hispanic) and non-Hispanic White women. Methods: In a subset of 4358 participants aged 35–74 years from the Sister Study, we estimated cross-sectional associations between self-reported use of four chemical hair products (permanent dye, semipermanent dye, straighteners/relaxers, and hair permanents/body waves) in the year before enrollment (2003–2009) and three DNA methylation-based measures of epigenetic age (DunedinPACE, GrimAge age acceleration [GrimAgeAccel], and PhenoAge age acceleration [PhenoAgeAccel]) using survey-weighted multivariable linear regressions. Associations were estimated both overall and by self-identified race and ethnicity, adjusting for chronological age, socioeconomic and lifestyle factors, body mass index, menopausal status, and DNA methylation platform. Results: Associations between the use of hair products and the three epigenetic age measures were largely null. Use of hair permanents/body waves was modestly associated with higher DunedinPACE among all participants (βever-never = 0.010; 95% confidence interval [CI] = 0.001, 0.019) and with lower PhenoAgeAccel among Black women (βever-never = −1.53; 95% CI = −2.84, −0.21). Conclusion: In this US-based study, we found little evidence of associations between chemical hair product use and epigenetic age in Black and non-Hispanic White women. Observed associations were modest and largely not supported by dose–response relationships or were inconsistent across epigenetic age measures. Previously observed associations between chemical hair product use and aging-related health outcomes may not be explained by the biological aging pathways captured by DunedinPACE, GrimAgeAccel, or PhenoAgeAccel. Alternative biological pathways are worth investigating in racially diverse samples.","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141126339","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}