Environmental Epidemiology最新文献

{"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}

{"title":"Hurricane Harvey and the risk of spontaneous preterm and early-term birth","authors":"Xinyue Liu, Alique G. Berberian, Sophia Wang, Lara J. Cushing","doi":"10.1097/EE9.0000000000000312","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000312","url":null,"abstract":"Background: Hurricane Harvey made landfall in August 2017 and resulted in catastrophic flooding in Houston, Texas. Prior studies of hurricanes and preterm birth have found conflicting results. We tested the hypotheses that exposure to Hurricane Harvey was associated with a higher risk of spontaneous pre- and early-term birth and assessed vulnerable subpopulations. Methods: We conducted a retrospective study of singleton births using administrative birth records in the nine-county greater Houston area from 2015 to 2019. We estimated the likelihood of pre- and early-term births using logistic regression, comparing births occurring during or within 1, 2, or 4 weeks of Hurricane Harvey to unexposed reference periods encompassing the same dates 2 years prior and after. Stratified models assessed effect modification by degree of flooding, birth parent age, high- vs. low-risk pregnancy, race/ethnicity, and prenatal care. Results: Among 15,564 births, we found no association between exposure to Hurricane Harvey and spontaneous preterm birth within 1 week adjusted (odds ratio [OR], 1.06; 95% confidence interval [CI] = 0.91, 1.25) but a 14% higher odds of spontaneous early-term birth (OR, 1.14; 95% CI = 1.04, 1.25). The odds of early-term birth were even higher in neighborhoods with severe flooding (OR, 1.21; 95% CI = 1.05, 1.38), segregated neighborhoods (OR, 1.23; 95% CI = 1.03, 1.47), and among foreign-born Hispanics (OR, 1.21; 95% CI = 1.04, 1.53) and pregnant people receiving no prenatal care (OR, 1.37; 95% CI = 1.03, 1.82). Effect estimates were attenuated or null when considering 2-week or 4-week lags to define exposure. Conclusions: Hurricane Harvey was associated with higher odds of spontaneous early-term birth up to 1 week later, especially among socially marginalized populations.","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":"141126532","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}

{"title":"Fine particulate matter air pollution and health implications for Nairobi, Kenya","authors":"Otienoh Oguge, Joshua Nyamondo, Noah Adera, Lydia Okolla, Beldine Okoth, Stephen Anyango, Augustine Afulo, A. Kumie, Jonathan Samet, Kiros Berhane","doi":"10.1097/ee9.0000000000000307","DOIUrl":"https://doi.org/10.1097/ee9.0000000000000307","url":null,"abstract":"\u0000 \u0000 Continuous ambient air quality monitoring in Kenya has been limited, resulting in a sparse data base on the health impacts of air pollution for the country. We have operated a centrally located monitor in Nairobi for measuring fine particulate matter (PM2.5), the pollutant that has demonstrated impact on health. Here, we describe the temporal levels and trends in PM2.5 data for Nairobi and evaluate associated health implications.\u0000 \u0000 \u0000 \u0000 We used a centrally located reference sensor, the beta attenuation monitor (BAM-1022), to measure hourly PM2.5 concentrations over a 3-year period (21 August 2019 to 20 August 2022). We used, at minimum, 75% of the daily hourly concentration to represent the 24-hour concentrations for a given calendar day. To estimate the deaths attributable to air pollution, we used the World Health Organization (WHO) AirQ+ tool with input as PM2.5 concentration data, local mortality statistics, and population sizes.\u0000 \u0000 \u0000 \u0000 The daily (24-hour) mean (±SEM) PM2.5 concentration was 19. 2 ± 0.6 (µg/m3). Pollutant levels were lowest at 03:00 and, peaked at 20:00. Sundays had the lowest daily concentrations, which increased on Mondays and remained high through Saturdays. By season, the pollutant concentrations were lowest in April and highest in August. The mean annual concentration was 18.4 ± 7.1 (µg/m3), which was estimated to lead to between 400 and 1,400 premature deaths of the city’s population in 2021 hence contributing 5%–8% of the 17,432 adult deaths excluding accidents when referenced to WHO recommended 2021 air quality guideline for annual thresholds of 5 µg/m3.\u0000 \u0000 \u0000 \u0000 Fine particulate matter air pollution in Nairobi showed daily, day-of-week, and seasonal fluctuations consistent with the anthropogenic source mix, particularly from motor vehicles. The long-term population exposure to PM2.5 was 3.7 times higher than the WHO annual guideline of 5 µg/m3 and estimated to lead to a substantial burden of attributable deaths. An updated regulation targeting measures to reduce vehicular emissions is recommended.\u0000","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140694622","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}

{"title":"An assessment of the mediating role of hypertension in the effect of long-term air pollution exposure on dementia","authors":"Tanya E. Libby, S. Ilango, C. Leary, E. Semmens, Claire E Adam, Annette L. Fitzpatrick, J. Kaufman, A. Hajat","doi":"10.1097/ee9.0000000000000306","DOIUrl":"https://doi.org/10.1097/ee9.0000000000000306","url":null,"abstract":"\u0000 \u0000 Growing evidence links air pollution exposure to the risk of dementia. We hypothesized that hypertension may partially mediate this effect.\u0000 \u0000 \u0000 \u0000 We previously documented an association between air pollution and dementia in the Ginkgo Evaluation of Memory Study, a randomized, placebo-controlled trial of 3069 adults ≥75 years across four US sites who were evaluated for dementia every 6 months from 2000–2008. We utilized a two-stage regression approach for causal mediation analysis to decompose the total effect of air pollution on dementia into its natural direct and indirect effect through prevalent hypertension. Exposure to air pollution in the 10 or 20 years before enrollment was assigned using estimates from fine-scale spatial-temporal models for PM2.5, PM10, and NO2. We used Poisson regression models for hypertension and Cox proportional hazard models for time-to-incident all-cause dementia, adjusting for a priori confounders.\u0000 \u0000 \u0000 \u0000 Participants were free of mild cognitive impairment at baseline (n = 2564 included in analyses); 69% had prevalent hypertension at baseline. During follow-up, 12% developed all-cause dementia (Alzheimer’s disease [AD] = 212; vascular dementia with or without AD [VaD/AD mixed] = 97). We did not find an adverse effect of any air pollutant on hypertension. Hypertension was associated with VaD/AD mixed (HR, 1.92 [95% CI = 1.14, 3.24]) but not AD. We did not observe mediation through hypertension for the effect of any pollutant on dementia outcomes.\u0000 \u0000 \u0000 \u0000 The lack of mediated effect may be due to other mechanistic pathways and the minimal effect of air pollution on hypertension in this cohort of older adults.\u0000","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140711235","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}

{"title":"Increased vascular stiffness in children exposed in utero but not children exposed postnatally to emissions from a coal mine fire","authors":"Emily J. Hemstock, Ashley Bigaran, S. Allgood, Amanda J. Wheeler, M. Dalton, Grant J. Williamson, Caroline X. Gao, Michael J. Abramson, Kazuaki Negishi, F. Johnston, G. Zosky","doi":"10.1097/ee9.0000000000000309","DOIUrl":"https://doi.org/10.1097/ee9.0000000000000309","url":null,"abstract":"\u0000 \u0000 Chronic, low-intensity air pollution exposure has been consistently associated with increased atherosclerosis in adults. However, there was limited research regarding the implications of acute, high-intensity air pollution exposure during childhood. We aimed to determine whether there were any associations between early-life exposure to such an episode and early-life vascular function changes.\u0000 \u0000 \u0000 \u0000 We conducted a prospective cohort study of children (<9 years old) who lived in the vicinity of the Hazelwood coal mine fire (n = 206). Vascular function was measured using noninvasive diagnostic methods including carotid intima-media thickness and pulse wave velocity (PWV). Exposure estimates were calculated from prognostic models and location diaries during the exposure period completed by each participant’s parent. Linear mixed-effects models were used to determine whether there were any associations between exposure and changes in vascular outcomes at the 3- and 7-year follow-ups and over time.\u0000 \u0000 \u0000 \u0000 At the 7-year follow-up, each 10 μg/m3 increase in daily PM2.5 in utero was associated with increased PWV (β = 0.13 m/s; 95% confidence interval [CI] = 0.02, 0.24; P = 0.02). The association between in utero exposure to daily PM2.5 was not altered by adjustment for covariates, body mass index, and maternal fire stress. Each 1 µg/m3 increase in background PM2.5 was associated with increased PWV (β = 0.68 m/s; 95% CI = 0.10, 1.26; P = 0.025), in children from the in utero exposure group. There was a trend toward smaller PWV (β = −0.17 m/s; 95% CI = −0.366, 0.02) from the 3- to 7-year follow-up clinic suggesting that the deficits observed previously in children exposed postnatally did not persist.\u0000 \u0000 \u0000 \u0000 There was a moderate improvement in vascular stiffness of children exposed to PM2.5 from a local coal mine fire in infancy. There was a mild increase in vascular stiffness in children exposed to PM2.5 from a local coal mine fire while their mothers were pregnant.\u0000","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140710507","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}

{"title":"Longitudinal associations between ambient PM_2.5 exposure and lipid levels in two Indian cities.","authors":"Kritika Anand, Gagandeep Kaur Walia, Siddhartha Mandal, Jyothi S Menon, Ruby Gupta, Nikhil Tandon, K M Venkat Narayan, Mohammed K Ali, Viswanathan Mohan, Joel D Schwartz, Dorairaj Prabhakaran","doi":"10.1097/EE9.0000000000000295","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000295","url":null,"abstract":"<p><strong>Background: </strong>Exposure to ambient PM_2.5 is known to affect lipid metabolism through systemic inflammation and oxidative stress. Evidence from developing countries, such as India with high levels of ambient PM_2.5 and distinct lipid profiles, is sparse.</p><p><strong>Methods: </strong>Longitudinal nonlinear mixed-effects analysis was conducted on >10,000 participants of Centre for cArdiometabolic Risk Reduction in South Asia (CARRS) cohort in Chennai and Delhi, India. We examined associations between 1-month and 1-year average ambient PM_2.5 exposure derived from the spatiotemporal model and lipid levels (total cholesterol [TC], triglycerides [TRIG], high-density lipoprotein cholesterol [HDL-C], and low-density lipoprotein cholesterol [LDL-C]) measured longitudinally, adjusting for residential and neighborhood-level confounders.</p><p><strong>Results: </strong>The mean annual exposure in Chennai and Delhi was 40 and 102 μg/m³ respectively. Elevated ambient PM_2.5 levels were associated with an increase in LDL-C and TC at levels up to 100 µg/m³ in both cities and beyond 125 µg/m³ in Delhi. TRIG levels in Chennai increased until 40 µg/m³ for both short- and long-term exposures, then stabilized or declined, while in Delhi, there was a consistent rise with increasing annual exposures. HDL-C showed an increase in both cities against monthly average exposure. HDL-C decreased slightly in Chennai with an increase in long-term exposure, whereas it decreased beyond 130 µg/m³ in Delhi.</p><p><strong>Conclusion: </strong>These findings demonstrate diverse associations between a wide range of ambient PM_2.5 and lipid levels in an understudied South Asian population. Further research is needed to establish causality and develop targeted interventions to mitigate the impact of air pollution on lipid metabolism and cardiovascular health.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11008625/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140850045","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}