Environmental Epidemiology最新文献

{"title":"Developmental language disorders in preschool children after high exposure to perfluoroalkyl substances from contaminated drinking water in Ronneby, Sweden.","authors":"Charlotte Stübner,&nbsp;Matilda Ebel,&nbsp;Kristina Jakobsson,&nbsp;Christopher Gillberg,&nbsp;Christel Nielsen,&nbsp;Carmela Miniscalco","doi":"10.1097/EE9.0000000000000233","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000233","url":null,"abstract":"<p><p>There are indications that early-life exposure to perfluoroalkyl substances (PFAS) can impact neurodevelopment, but results are inconclusive. The objective was to investigate if high early-life exposure to primarily perfluorohexanesulfonic acid (PFHxS) and perfluorooctanesulfonic acid (PFOS) increases the risk of developmental language disorder in children up to seven years of age.</p><p><strong>Methods: </strong>A register-based cohort of all children born 1998-2013 in Blekinge county, Sweden, was studied. Maternal residential history, that is, with or without highly PFAS-contaminated drinking water, during the 5-year period before childbirth was used as a proxy for early-life exposure. Exposure was categorized as high (n = 646), intermediate (n = 1,650), or background (n = 9,599). We used Cox proportional hazards regression to estimate hazard ratios (HR) for (1) referral to a speech- and language pathologist after routine screening at Child Health Services, and (2) subsequent language disorder diagnosis after clinical assessment. Models were adjusted for parity, maternal age, education level, and smoking, and explored effect modification by sex.</p><p><strong>Results: </strong>In children from the high-exposed area, the adjusted HR for referral was 1.23 (95% CI = 1.03, 1.47) and 1.13 (95% CI = 0.97, 1.56) for subsequent diagnosis. There was no increased risk in the intermediate exposure category.</p><p><strong>Conclusion: </strong>Children, particularly girls, with high exposure had an increased risk of both referral and confirmed developmental language disorder. Further research is needed on PFAS in the context of general neurodevelopment, for which language development is a proxy.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/2e/26/ee9-7-e233.PMC9916036.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10765263","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":"Exposure to ultrafine particles and the incidence of asthma in children: A population-based cohort study in Montreal, Canada.","authors":"Alan da Silveira Fleck,&nbsp;Julien Vachon,&nbsp;Stéphane Buteau,&nbsp;Elhadji Anassour Laouan-Sidi,&nbsp;Marianne Hatzopoulou,&nbsp;Scott Weichenthal,&nbsp;Audrey Smargiassi","doi":"10.1097/EE9.0000000000000236","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000236","url":null,"abstract":"<p><p>Asthma is the most prevalent chronic respiratory disease in children. The role of ultrafine particles (UFPs) in the development of the disease remains unclear. We used a population-based birth cohort to evaluate the association between prenatal and childhood exposure to low levels of ambient UFPs and childhood-onset asthma.</p><p><strong>Methods: </strong>The cohort included all children born and residing in Montreal, Canada, between 2000 and 2015. Children were followed for asthma onset from birth until <13 years of age. Spatially resolved annual mean concentrations of ambient UFPs were estimated from a land use regression model. We assigned prenatal exposure according to the residential postal code at birth. We also considered current exposure during childhood accounting for time-varying residence location. We estimated hazard ratios (HRs) using Cox proportional hazards models adjusted for age, sex, neighborhood material and social deprivation, calendar year, and coexposure to ambient nitrogen dioxide (NO₂) and fine particles (PM_2.5).</p><p><strong>Results: </strong>The cohort included 352,966 children, with 30,825 children developing asthma during follow-up. Mean prenatal and childhood UFP exposure were 24,706 particles/cm³ (interquartile range [IQR] = 3,785 particles/cm³) and 24,525 particles/cm³ (IQR = 3,427 particles/cm³), respectively. Both prenatal and childhood UFP exposure were not associated with childhood asthma onset in single pollutant models (HR per IQR increase of 0.99 [95% CI = 0.98, 1.00]). Estimates of association remained similar when adjusting for coexposure to ambient NO₂ and PM_2.5.</p><p><strong>Conclusion: </strong>In this population-based birth cohort, childhood asthma onset was not associated with prenatal or childhood exposure to low concentrations of UFPs.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/24/ee/ee9-7-e236.PMC9916019.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9259634","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":"Erratum: Neighborhood conditions and birth outcomes: understanding the role of perceived and extrinsic measures of neighborhood quality: Erratum.","authors":"","doi":"10.1097/EE9.0000000000000240","DOIUrl":"10.1097/EE9.0000000000000240","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1097/EE9.0000000000000224.].</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2023-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/43/0c/ee9-7-e240.PMC9916117.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9259640","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 early-life exposure to PM_2.5 and reductions in childhood lung function in two North American longitudinal pregnancy cohort studies.","authors":"Maria José Rosa, Hector Lamadrid-Figueroa, Cecilia Alcala, Elena Colicino, Marcela Tamayo-Ortiz, Adriana Mercado-Garcia, Itai Kloog, Allan C Just, Douglas Bush, Kecia N Carroll, Martha María Téllez-Rojo, Robert O Wright, Chris Gennings, Rosalind J Wright","doi":"10.1097/EE9.0000000000000234","DOIUrl":"10.1097/EE9.0000000000000234","url":null,"abstract":"<p><p>Data integration of epidemiologic studies across different geographic regions can provide enhanced exposure contrast and statistical power to examine adverse respiratory effects of early-life exposure to particulate matter <2.5 microns in diameter (PM_2.5). Methodological tools improve our ability to combine data while more fully accounting for study heterogeneity.</p><p><strong>Methods: </strong>Analyses included children enrolled in two longitudinal birth cohorts in Boston, Massachusetts, and Mexico City. Propensity score matching using the 1:3 nearest neighbor with caliper method was used. Residential PM_2.5 exposure was estimated from 2 months before birth to age 6 years using a validated satellite-based spatiotemporal model. Lung function was tested at ages 6-11 years and age, height, race, and sex adjusted z scores were estimated for FEV₁, FVC, FEF_25-75%, and FEV₁/FVC. Using distributed lag nonlinear models, we examined associations between monthly averaged PM_2.5 levels and lung function outcomes adjusted for covariates, in unmatched and matched pooled samples.</p><p><strong>Results: </strong>In the matched pooled sample, PM_2.5 exposure between postnatal months 35-44 and 35-52 was associated with lower FEV₁ and FVC z scores, respectively. A 5 µg/m³ increase in PM_2.5 was associated with a reduction in FEV₁ z score of 0.13 (95% CI = -0.26, -0.01) and a reduction in FVC z score of 0.13 (95% CI = -0.25, -0.01). Additionally PM_2.5 during postnatal months 23-39 was associated with a reduction in FEF_25-75% z score of 0.31 (95% CI = -0.57, -0.05).</p><p><strong>Conclusions: </strong>Methodological tools enhanced our ability to combine multisite data while accounting for study heterogeneity. Ambient PM_2.5 exposure in early childhood was associated with lung function reductions in middle childhood.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/84/85/ee9-7-e234.PMC9915957.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9477208","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":"Neighborhood socioeconomic status and mortality in the nurses' health study (NHS) and the nurses' health study II (NHSII).","authors":"Nicole V DeVille, Hari S Iyer, Isabel Holland, Shilpa N Bhupathiraju, Boyang Chai, Peter James, Ichiro Kawachi, Francine Laden, Jaime E Hart","doi":"10.1097/EE9.0000000000000235","DOIUrl":"10.1097/EE9.0000000000000235","url":null,"abstract":"<p><p>Few studies have prospectively examined long-term associations between neighborhood socioeconomic status (nSES) and mortality risk, independent of demographic and lifestyle risk factors.</p><p><strong>Methods: </strong>We assessed associations between nSES and all-cause, nonaccidental mortality among women in the Nurses' Health Study (NHS) 1986-2014 (N = 101,701) and Nurses' Health Study II (NHSII) 1989-2015 (N = 101,230). Mortality was ascertained from the National Death Index (NHS: 19,228 deaths; NHSII: 1556 deaths). Time-varying nSES was determined for the Census tract of each residential address. We used principal component analysis (PCA) to identify nSES variable groups. Multivariable Cox proportional hazards models were conditioned on age and calendar period and included time-varying demographic, lifestyle, and individual SES factors.</p><p><strong>Results: </strong>For NHS, hazard ratios (HRs) comparing the fifth to first nSES quintiles ranged from 0.89 (95% confidence interval [CI] = 0.84, 0.94) for percent of households receiving interest/dividends, to 1.11 (95% CI = 1.06, 1.17) for percent of households receiving public assistance income. In NHSII, HRs ranged from 0.72 (95% CI: 0.58, 0.88) for the percent of households receiving interest/dividends, to 1.27 (95% CI: 1.07, 1.49) for the proportion of households headed by a single female. PCA revealed three constructs: education/income, poverty/wealth, and racial composition. The racial composition construct was associated with mortality (HR_NHS: 1.03; 95% CI = 1.01, 1.04).</p><p><strong>Conclusion: </strong>In two cohorts with extensive follow-up, individual nSES variables and PCA component scores were associated with mortality. nSES is an important population-level predictor of mortality, even among a cohort of women with little individual-level variability in SES.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2022-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/87/28/ee9-7-e235.PMC9916023.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10765261","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":"Early-life exposure to per- and polyfluoroalkyl substances and infant gut microbial composition.","authors":"Hannah E Laue, Yuka Moroishi, Thomas J Palys, Brock C Christensen, Rachel L Criswell, Lisa A Peterson, Carin A Huset, Emily R Baker, Margaret R Karagas, Juliette C Madan, Megan E Romano","doi":"10.1097/EE9.0000000000000238","DOIUrl":"10.1097/EE9.0000000000000238","url":null,"abstract":"<p><p>Human milk is rich in essential nutrients and immune-activating compounds but is also a source of toxicants including per- and polyfluoroalkyl substances (PFAS). Evidence suggests that immune-related effects of PFAS may, in part, be due to alterations of the microbiome. We aimed to identify the association between milk PFAS exposure and the infant gut microbiome.</p><p><strong>Methods: </strong>PFAS [perfluorooctane sulfonic acid (PFOS) and perfluorooctanoate (PFOA)] were quantified in milk from ~6 weeks postpartum using high-performance liquid chromatography with tandem mass spectrometry. A molar sum (ΣPFAS) was calculated. Caregivers collected infant stool samples at 6 weeks (n = 116) and/or 1 year postpartum (n = 119). Stool DNA underwent metagenomic sequencing. We estimated the association of PFAS with diversity and relative abundances of species with linear regression. Single- and multi-PFAS models adjusted for potential confounders in complete case analyses and with imputed missing covariate data for 6-week and 1-year microbiomes separately. We assessed sensitive populations with stratification.</p><p><strong>Results: </strong>PFOS and PFOA were detected in 94% and 83% of milk samples, respectively. PFOS was associated with increased diversity at 6 weeks among infants fed exclusively human milk [β = 0.24 per PFOS doubling, (95% CI = 0.03, 0.45), <i>P</i> = 0.03] and born to primiparous mothers [β = 0.37 (0.06, 0.67), <i>P</i> = 0.02]. Estimates were strongest in multi-PFAS models and among complete cases. ΣPFAS was associated with <i>Bacteroides vulgatus</i> relative abundance at 1 year [(β = -2.34% per doubling (-3.63, -1.05), FDR q = 0.099].</p><p><strong>Conclusions: </strong>PFAS may increase infant gut microbiome diversity and alter the relative abundance of biologically relevant bacteria. Additional analyses may identify related health outcomes.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2022-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/00/cd/ee9-7-e238.PMC9916123.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9259642","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":"Inherited genetic effects on arsenic metabolism: A comparison of effects on arsenic species measured in urine and in blood.","authors":"Lizeth I Tamayo,&nbsp;Yohhan Kumarasinghe,&nbsp;Lin Tong,&nbsp;Olgica Balac,&nbsp;Habibul Ahsan,&nbsp;Mary Gamble,&nbsp;Brandon L Pierce","doi":"10.1097/EE9.0000000000000230","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000230","url":null,"abstract":"<p><p>Inorganic arsenic (iAs) is a carcinogen, and chronic exposure is associated with adverse health outcomes, including cancer and cardiovascular disease. Consumed iAs can undergo two methylation reactions catalyzed by arsenic methyltransferase (<i>AS3MT</i>), producing monomethylated and dimethylated forms of arsenic (MMA and DMA). Methylation of iAs helps facilitate excretion of arsenic in urine, with DMA composing the majority of arsenic species excreted. Past studies have identified genetic variation in the <i>AS3MT</i> (10q24.32) and <i>FTCD</i> (21q22.3) regions associated with arsenic metabolism efficiency (AME), measured as the proportion of each species present in urine (iAs%, MMA%, and DMA%), but their association with arsenic species present in blood has not been examined. We use data from three studies nested within the Health Effects and Longitudinal Study (HEALS)-the Nutritional Influences on Arsenic Toxicity Study, the Folate and Oxidative Stress study, and the Folic Acid and Creatine Trial-to examine the association of previously identified genetic variants with arsenic species in both urine and blood of 334 individuals. We confirm that the genetic variants in <i>AS3MT</i> and <i>FTCD</i> known to effect arsenic species composition in urine (an excreted byproduct of metabolism) have similar effects on arsenic species in blood (a tissue type that directly interacts with many organs, including those prone to arsenic toxicity). This consistency we observe provides further support for the hypothesis the AME SNPs identified to date impact the efficiency of arsenic metabolism and elimination, thereby influencing internal dose of arsenic and the dose delivered to toxicity-prone organs and tissues.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9746746/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9595118","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":"Sensitivity analysis for live birth bias in the Ulaanbaatar Gestation and Air Pollution Research study.","authors":"Lawrence C McCandless,&nbsp;Enkhjargal Gombojav,&nbsp;Ryan W Allen","doi":"10.1097/EE9.0000000000000229","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000229","url":null,"abstract":"<p><p>The Ulaanbaatar Gestation and Air Pollution Research (UGAAR) study is a randomized controlled trial of the effects of portable high efficiency particulate air (HEPA) filter air cleaner use during pregnancy on fetal growth and child health outcomes. A challenge with the study is that the outcome variables cannot be measured in the absence of a live birth. Thus pregnancy loss is a competing event for the outcome variables that can obscure the intervention-outcome relationship. This phenomenon is called \"live birth bias\" in the epidemiological literature, and it is an example of selection bias due to adjustment for variables affected by previous exposure.</p><p><strong>Methods: </strong>In this investigation, we reanalyzed data from the UGAAR study and examined the impacts of the intervention on three health outcomes: preterm birth (PTB), birth weight, and full-scale IQ (FSIQ) measured with the Wechsler Preschool and Primary Scale of Intelligence III when children were four years old, while accounting for live birth bias. Specifically, we used a novel multiple imputation approach to simulate scenarios in which pregnancy losses had instead been born alive and experienced a range of health outcomes.</p><p><strong>Results: </strong>After accounting for live birth bias, the association between the intervention and PTB diminished. Additionally, the magnitude of intervention effect on birth weight and FSIQ increased. FSIQ was less sensitive to live birth bias than birth weight.</p><p><strong>Conclusion: </strong>We introduced a novel analysis approach to examine the role of live birth bias, and the findings will be useful in environmental epidemiology studies of birth cohorts.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/1d/f0/ee9-6-e229.PMC9746740.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10404440","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":"Lagged acute respiratory outcomes among children related to ambient pollutant exposure in a high exposure setting in South Africa.","authors":"Shumani Phaswana,&nbsp;Caradee Y Wright,&nbsp;Rebecca M Garland,&nbsp;Thulie N Khumalo,&nbsp;Rajen N Naidoo","doi":"10.1097/EE9.0000000000000228","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000228","url":null,"abstract":"<p><p>Acute ambient air pollution impacts on the respiratory health of children may be lagged across time. We determined the short-term lagged effects of particulate matter (PM_2.5), sulphur dioxide (SO₂), and oxides of nitrogen (NO_x) on the respiratory health of children living in low-income communities.</p><p><strong>Methods: </strong>A school-based study was conducted using a repeated measures design, across summer and winter, in four schools in each of four suburbs in the Vaal Triangle, South Africa. Data for PM_2.5, NO_x, and SO₂ were obtained from monitoring stations within close proximity of the schools. Over 10 school days in each phase, grade 4 children completed a symptoms log and lung function tests. Parents completed a child respiratory questionnaire. Generalized estimation equations models adjusted for covariates of interest in relation to lung function outcomes and air pollutants including lag effects of 1-5 days.</p><p><strong>Results: </strong>Daily PM_2.5, NO_x, and SO₂ median concentration levels were frequently higher than international standards. Among the 280 child participants (mean age 9 years), the prevalence of symptoms based on probable asthma was 9.6%. There was a consistent increased pollutant-related risk for respiratory symptoms, except for NO_x and shortness of breath. Lung function, associated with pollutant fluctuations across the different lags, was most pronounced for peak expiratory flow rate (PEFR) for PM_2.5 and SO₂. A preceding 5-day average SO₂ exposure had the largest loss (7.5 L/minute) in PEFR.</p><p><strong>Conclusions: </strong>Lagged declines in daily lung function and increased odds of having respiratory symptoms were related to increases in PM_2.5 and SO₂ among a school-based sample of children.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9746739/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10400202","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":"Ambient exposures to selected volatile organic compounds and the risk of prostate cancer in Montreal.","authors":"Mark S Goldberg, Sara Zapata-Marin, France Labrèche, Vikki Ho, Eric Lavigne, Marie-France Valois, Marie-Elise Parent","doi":"10.1097/EE9.0000000000000231","DOIUrl":"10.1097/EE9.0000000000000231","url":null,"abstract":"<p><p>Little is known about environmental factors that may increase the risk of prostate cancer. We estimated associations between incident prostate cancer and environmental concentrations of five ambient volatile organic compounds (VOCs): benzene; n-decane; ethylbenzene; hexane; and 1,2,4-trimethylbenzene.</p><p><strong>Methods: </strong>This study is based on a population-based case-control study of incident prostate cancer (PROtEuS) in men ≤ 75 years of age living in Montreal, Canada, in 2005 to 2012. We included 1172 cases and 1177 population controls. We had personal information, lifetime residential addresses, occupational exposures, and a variety of area-wide covariables. We inferred concentrations of the five VOCs using Bayesian geostatistical models using data from a dense environmental survey conducted in Montreal in 2005 to 2006. We used different sets of adjustments to estimate odds ratios (OR) and confidence intervals.</p><p><strong>Results: </strong>We found nonlinear associations such that the ORs increased monotonically and then either flattened or fell off with increased exposures. The model that contained other environmental variables and contextual variables led to lower ORs and results were similar when we restricted analyses to controls recently screened or tested for prostate cancer or cases with low- or high-grade tumors. A change from the 5th to 25th percentile in mean environmental benzene levels led to an adjusted OR of 2.00 (95% confidence interval = 1.47, 2.71).</p><p><strong>Conclusion: </strong>We found positive associations between prostate cancer and concentrations of benzene and ethylbenzene, independently of previous testing for prostate cancer or tumor grade, suggesting that exposure to certain ambient VOCs may increase incidence.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/59/82/ee9-6-e231.PMC9746733.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10404439","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}