Pub Date : 2022-09-14eCollection Date: 2022-10-01DOI: 10.1097/EE9.0000000000000226
Sara Zapata-Marin, Alexandra M Schmidt, Dan Crouse, Vikki Ho, France Labrèche, Eric Lavigne, Marie-Élise Parent, Mark S Goldberg
Volatile organic compounds (VOCs) are components of the complex mixture of air pollutants within cities and can cause various adverse health effects. Therefore, it is necessary to understand their spatial distribution for exposure assessment in epidemiological studies.
Objectives: The objective was to model measured concentrations of five VOCs within the city of Montreal, Canada, developing spatial prediction models that can be used in health studies.
Methods: We measured concentrations using 3M 3500 Organic Vapor Monitors, over 2-week periods, for three monitoring campaigns between 2005 and 2006 in over 130 locations in the city. Using GC/MSD (Gas Chromatography/Mass Selective Detector), we measured concentrations of benzene, n-decane, ethylbenzene, hexane, and trimethylbenzene. We fitted four different models that combine land-use regression and geostatistical methods to account for the potential spatial structure that remains after accounting for the land-use variables. The fitted models also accounted for possible variations in the concentration of air pollutants across campaigns.
Results: The highest concentrations for all VOCs were found in December with hexane being the most abundant followed by ethylbenzene. We obtained predicted surfaces for the VOCs for the three campaigns and mean surfaces across campaigns. We found higher concentrations of some VOCs along highways and in the Eastern part of Montreal, which is a highly industrialized area.
Conclusions: Each of the fitted models captured the spatial and across-campaigns variability for each VOC, and we found that different VOCs required different model structures.
{"title":"Spatial modeling of ambient concentrations of volatile organic compounds in Montreal, Canada.","authors":"Sara Zapata-Marin, Alexandra M Schmidt, Dan Crouse, Vikki Ho, France Labrèche, Eric Lavigne, Marie-Élise Parent, Mark S Goldberg","doi":"10.1097/EE9.0000000000000226","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000226","url":null,"abstract":"<p><p>Volatile organic compounds (VOCs) are components of the complex mixture of air pollutants within cities and can cause various adverse health effects. Therefore, it is necessary to understand their spatial distribution for exposure assessment in epidemiological studies.</p><p><strong>Objectives: </strong>The objective was to model measured concentrations of five VOCs within the city of Montreal, Canada, developing spatial prediction models that can be used in health studies.</p><p><strong>Methods: </strong>We measured concentrations using 3M 3500 Organic Vapor Monitors, over 2-week periods, for three monitoring campaigns between 2005 and 2006 in over 130 locations in the city. Using GC/MSD (Gas Chromatography/Mass Selective Detector), we measured concentrations of benzene, n-decane, ethylbenzene, hexane, and trimethylbenzene. We fitted four different models that combine land-use regression and geostatistical methods to account for the potential spatial structure that remains after accounting for the land-use variables. The fitted models also accounted for possible variations in the concentration of air pollutants across campaigns.</p><p><strong>Results: </strong>The highest concentrations for all VOCs were found in December with hexane being the most abundant followed by ethylbenzene. We obtained predicted surfaces for the VOCs for the three campaigns and mean surfaces across campaigns. We found higher concentrations of some VOCs along highways and in the Eastern part of Montreal, which is a highly industrialized area.</p><p><strong>Conclusions: </strong>Each of the fitted models captured the spatial and across-campaigns variability for each VOC, and we found that different VOCs required different model structures.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":" ","pages":"e226"},"PeriodicalIF":3.6,"publicationDate":"2022-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/c2/d4/ee9-6-e226.PMC9555929.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33545198","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}
Pub Date : 2022-09-02eCollection Date: 2022-10-01DOI: 10.1097/EE9.0000000000000220
Ettie M Lipner, Joshua P French, Stephen Nelson, Joseph O Falkinham Iii, Rachel A Mercaldo, Rebekah A Blakney, Yihe G Daida, Timothy B Frankland, Kyle P Messier, Jennifer R Honda, Stacey Honda, D Rebecca Prevots
Hawai'i has the highest prevalence of nontuberculous mycobacterial (NTM) pulmonary disease in the United States. Previous studies indicate that certain trace metals in surface water increase the risk of NTM infection.
Objective: To identify whether trace metals influence the risk of NTM infection in O'ahu, Hawai'i.
Methods: A population-based ecologic cohort study was conducted using NTM infection incidence data from patients enrolled at Kaiser Permanente Hawai'i during 2005-2019. We obtained sociodemographic, microbiologic, and geocoded residential data for all Kaiser Permanente Hawai'i beneficiaries. To estimate the risk of NTM pulmonary infection from exposure to groundwater constituents, we obtained groundwater data from three data sources: (1) Water Quality Portal; (2) the Hawai'i Department of Health; and (3) Brigham Young University, Department of Geological Science faculty. Data were aggregated by an aquifer and were associated with the corresponding beneficiary aquifer of residence. We used Poisson regression models with backward elimination to generate models for NTM infection risk as a function of groundwater constituents. We modeled two outcomes: Mycobacterium avium complex (MAC) species and Mycobacterium abscessus group species.
Results: For every 1-unit increase in the log concentration of vanadium in groundwater at the aquifer level, infection risk increased by 22% among MAC patients. We did not observe significant associations between water-quality constituents and infection risk among M. abscessus patients.
Conclusions: Concentrations of vanadium in groundwater were associated with MAC pulmonary infection in O'ahu, Hawai'i. These findings provide evidence that naturally occurring trace metals influence the presence of NTM in water sources that supply municipal water systems.
{"title":"Vanadium in groundwater aquifers increases the risk of MAC pulmonary infection in O'ahu, Hawai'i.","authors":"Ettie M Lipner, Joshua P French, Stephen Nelson, Joseph O Falkinham Iii, Rachel A Mercaldo, Rebekah A Blakney, Yihe G Daida, Timothy B Frankland, Kyle P Messier, Jennifer R Honda, Stacey Honda, D Rebecca Prevots","doi":"10.1097/EE9.0000000000000220","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000220","url":null,"abstract":"<p><p>Hawai'i has the highest prevalence of nontuberculous mycobacterial (NTM) pulmonary disease in the United States. Previous studies indicate that certain trace metals in surface water increase the risk of NTM infection.</p><p><strong>Objective: </strong>To identify whether trace metals influence the risk of NTM infection in O'ahu, Hawai'i.</p><p><strong>Methods: </strong>A population-based ecologic cohort study was conducted using NTM infection incidence data from patients enrolled at Kaiser Permanente Hawai'i during 2005-2019. We obtained sociodemographic, microbiologic, and geocoded residential data for all Kaiser Permanente Hawai'i beneficiaries. To estimate the risk of NTM pulmonary infection from exposure to groundwater constituents, we obtained groundwater data from three data sources: (1) Water Quality Portal; (2) the Hawai'i Department of Health; and (3) Brigham Young University, Department of Geological Science faculty. Data were aggregated by an aquifer and were associated with the corresponding beneficiary aquifer of residence. We used Poisson regression models with backward elimination to generate models for NTM infection risk as a function of groundwater constituents. We modeled two outcomes: <i>Mycobacterium avium</i> complex (MAC) species and <i>Mycobacterium abscessus</i> group species.</p><p><strong>Results: </strong>For every 1-unit increase in the log concentration of vanadium in groundwater at the aquifer level, infection risk increased by 22% among MAC patients. We did not observe significant associations between water-quality constituents and infection risk among <i>M. abscessus</i> patients.</p><p><strong>Conclusions: </strong>Concentrations of vanadium in groundwater were associated with MAC pulmonary infection in O'ahu, Hawai'i. These findings provide evidence that naturally occurring trace metals influence the presence of NTM in water sources that supply municipal water systems.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":" ","pages":"e220"},"PeriodicalIF":3.6,"publicationDate":"2022-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9555944/pdf/ee9-6-e220.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33516650","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}
Pub Date : 2022-08-31eCollection Date: 2022-10-01DOI: 10.1097/EE9.0000000000000221
Barbara Hoffmann, Bert Brunekreef, Zorana J Andersen, Francesco Forastiere, Hanna Boogaard
Health impact assessments (HIA) and cost-benefit analyses (CBA) play a major role in the ongoing revision of the European Union Ambient Air Quality Directive (EU AAQD). HIAs quantify the public health impacts of the air pollution levels a population is exposed to. CBAs quantify the economic costs of achieving lower air pollution levels and the (monetized) benefits for public health that result from these lower air pollution levels. In this commentary, we consider the recent body of evidence on the effects of long-term exposure to fine particulate matter (PM2.5) and nitrogen dioxide (NO2) on total mortality from natural causes and present the rationale for conducting additional analyses within the framework of the HIA conducted for the revision of the EU AAQD, based on the recently published European “Effects of Low-Level Air Pollution: A Study in Europe” (ELAPSE) study. The air pollution-related burden (presented as impact on mortality from natural causes) for Europe has been estimated since 2014 in the annual “Air Quality in Europe” reports published by the European Environment Agency (EEA). EEA in their HIA has used relative risk estimates from meta-analyses by Hoek and colleagues1 in 2013, based on evidence published before January 2013: 1.06 (1.04, 1.08) for PM2.5 and 1.05 (1.03, 1.08) for NO2, both per 10 μg/m 3. The EEA, in its latest HIA for 2019, assumed no threshold for PM2.5, and a threshold of 20 μg/m3 for NO2, and estimated 307,000 and 40,400 premature deaths in the EU27 associated with PM2.5 and NO2, respectively. 2 In support of the recent development of the 2021 World Health Organization (WHO) Air Quality Guidelines, new systematic reviews of the evidence of effects of air pollutants on mortality were published in 2020.3,4 These reviews include studies conducted in all parts of the world and across a wide range of exposure levels. The linear summary estimates from these global systematic reviews are used in the current HIA and CBA informing the revision of the EU AAQD. The systematic review on PM2.5 and total mortality documented a summary estimate of 1.08 per 10 μg/m3 with a confidence interval of (1.06, 1.09), based on 25 studies.3 The systematic review on NO2 and total mortality reported a summary estimate of 1.02 per 10 μg/m3 with a confidence interval of (1.01, 1.04), based on 24 studies.4 This latter review has also reported an association between longterm, warm season ozone exposure and total mortality with a summary effect estimate of 1.01 (1.00, 1.02) per 10 μg/m3, which is being used to estimate the impacts of long-term warm season ozone concentrations in the revision of the EU AAQD. These systematic reviews were published in 2020 and included studies available until September 2018. They do not include important new European studies that have been published since. We propose that additional analyses should be conducted based on these new studies to ensure that the HIA and CBA to inform the revision of the EU AAQD consider
{"title":"Benefits of future clean air policies in Europe: Proposed analyses of the mortality impacts of PM<sub>2.5</sub> and NO<sub>2</sub>.","authors":"Barbara Hoffmann, Bert Brunekreef, Zorana J Andersen, Francesco Forastiere, Hanna Boogaard","doi":"10.1097/EE9.0000000000000221","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000221","url":null,"abstract":"Health impact assessments (HIA) and cost-benefit analyses (CBA) play a major role in the ongoing revision of the European Union Ambient Air Quality Directive (EU AAQD). HIAs quantify the public health impacts of the air pollution levels a population is exposed to. CBAs quantify the economic costs of achieving lower air pollution levels and the (monetized) benefits for public health that result from these lower air pollution levels. In this commentary, we consider the recent body of evidence on the effects of long-term exposure to fine particulate matter (PM2.5) and nitrogen dioxide (NO2) on total mortality from natural causes and present the rationale for conducting additional analyses within the framework of the HIA conducted for the revision of the EU AAQD, based on the recently published European “Effects of Low-Level Air Pollution: A Study in Europe” (ELAPSE) study. The air pollution-related burden (presented as impact on mortality from natural causes) for Europe has been estimated since 2014 in the annual “Air Quality in Europe” reports published by the European Environment Agency (EEA). EEA in their HIA has used relative risk estimates from meta-analyses by Hoek and colleagues1 in 2013, based on evidence published before January 2013: 1.06 (1.04, 1.08) for PM2.5 and 1.05 (1.03, 1.08) for NO2, both per 10 μg/m 3. The EEA, in its latest HIA for 2019, assumed no threshold for PM2.5, and a threshold of 20 μg/m3 for NO2, and estimated 307,000 and 40,400 premature deaths in the EU27 associated with PM2.5 and NO2, respectively. 2 In support of the recent development of the 2021 World Health Organization (WHO) Air Quality Guidelines, new systematic reviews of the evidence of effects of air pollutants on mortality were published in 2020.3,4 These reviews include studies conducted in all parts of the world and across a wide range of exposure levels. The linear summary estimates from these global systematic reviews are used in the current HIA and CBA informing the revision of the EU AAQD. The systematic review on PM2.5 and total mortality documented a summary estimate of 1.08 per 10 μg/m3 with a confidence interval of (1.06, 1.09), based on 25 studies.3 The systematic review on NO2 and total mortality reported a summary estimate of 1.02 per 10 μg/m3 with a confidence interval of (1.01, 1.04), based on 24 studies.4 This latter review has also reported an association between longterm, warm season ozone exposure and total mortality with a summary effect estimate of 1.01 (1.00, 1.02) per 10 μg/m3, which is being used to estimate the impacts of long-term warm season ozone concentrations in the revision of the EU AAQD. These systematic reviews were published in 2020 and included studies available until September 2018. They do not include important new European studies that have been published since. We propose that additional analyses should be conducted based on these new studies to ensure that the HIA and CBA to inform the revision of the EU AAQD consider","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":" ","pages":"e221"},"PeriodicalIF":3.6,"publicationDate":"2022-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/5a/49/ee9-6-e221.PMC9556041.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33516652","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}
Pub Date : 2022-08-31eCollection Date: 2022-10-01DOI: 10.1097/EE9.0000000000000222
Yu Zhang, Vicente Mustieles, Paige L Williams, Irene Souter, Antonia M Calafat, Melina Demokritou, Alexandria Lee, Stylianos Vagios, Russ Hauser, Carmen Messerlian
Although parental preconception exposure to some phenols and phthalates have been associated with reduced birthweight, few studies have examined these chemicals as complex mixtures.
Methods: We included 384 mothers and 211 fathers (203 couples) who gave birth to 384 singletons from a prospective cohort of couples seeking fertility evaluation. Urinary concentrations of bisphenol A (BPA), parabens, and 11 phthalate metabolites including those of di(2-ethylhexyl) phthalate (DEHP) were examined. Birthweight was abstracted from delivery records. We used principal component analysis and Bayesian Kernel Machine Regression (BKMR) to examine maternal and paternal preconception mixtures in relation to singleton birthweight. We also fit couple-based BKMR with hierarchical variable selection to assess couples' joint mixtures in relation to birthweight.
Results: PC scores of maternal and paternal preconception low molecular weight phthalates factor, and paternal preconception DEHP-BPA factor were associated with reduced birthweight. In BKMR models, we found that maternal preconception monoethyl phthalate and BPA concentrations, and paternal preconception mono-n-butyl phthalate concentrations were inversely associated with birthweight when the remaining mixture components were held at their median concentrations. In couple-based BKMR models, paternal preconception biomarkers contributed more to couples' joint effect on birthweight compared with maternal preconception biomarkers. A decreasing trend of birthweight was observed across quantiles of maternal, paternal, and couples' total preconception mixture concentrations, respectively.
Conclusions: Results from this preconception cohort of subfertile couples suggest a complex interplay between paternal and maternal preconception exposure to mixtures of nonpersistent chemicals, with both parental windows of exposure jointly contributing to reduced birthweight.
{"title":"Association of preconception mixtures of phenol and phthalate metabolites with birthweight among subfertile couples.","authors":"Yu Zhang, Vicente Mustieles, Paige L Williams, Irene Souter, Antonia M Calafat, Melina Demokritou, Alexandria Lee, Stylianos Vagios, Russ Hauser, Carmen Messerlian","doi":"10.1097/EE9.0000000000000222","DOIUrl":"10.1097/EE9.0000000000000222","url":null,"abstract":"<p><p>Although parental preconception exposure to some phenols and phthalates have been associated with reduced birthweight, few studies have examined these chemicals as complex mixtures.</p><p><strong>Methods: </strong>We included 384 mothers and 211 fathers (203 couples) who gave birth to 384 singletons from a prospective cohort of couples seeking fertility evaluation. Urinary concentrations of bisphenol A (BPA), parabens, and 11 phthalate metabolites including those of di(2-ethylhexyl) phthalate (DEHP) were examined. Birthweight was abstracted from delivery records. We used principal component analysis and Bayesian Kernel Machine Regression (BKMR) to examine maternal and paternal preconception mixtures in relation to singleton birthweight. We also fit couple-based BKMR with hierarchical variable selection to assess couples' joint mixtures in relation to birthweight.</p><p><strong>Results: </strong>PC scores of maternal and paternal preconception low molecular weight phthalates factor, and paternal preconception DEHP-BPA factor were associated with reduced birthweight. In BKMR models, we found that maternal preconception monoethyl phthalate and BPA concentrations, and paternal preconception mono-n-butyl phthalate concentrations were inversely associated with birthweight when the remaining mixture components were held at their median concentrations. In couple-based BKMR models, paternal preconception biomarkers contributed more to couples' joint effect on birthweight compared with maternal preconception biomarkers. A decreasing trend of birthweight was observed across quantiles of maternal, paternal, and couples' total preconception mixture concentrations, respectively.</p><p><strong>Conclusions: </strong>Results from this preconception cohort of subfertile couples suggest a complex interplay between paternal and maternal preconception exposure to mixtures of nonpersistent chemicals, with both parental windows of exposure jointly contributing to reduced birthweight.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":" ","pages":"e222"},"PeriodicalIF":3.8,"publicationDate":"2022-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9555928/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33516649","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}
Pub Date : 2022-08-23eCollection Date: 2022-10-01DOI: 10.1097/EE9.0000000000000223
Vanessa R Coffman, Anja Søndergaard Jensen, Betina B Trabjerg, Carsten Bøcker Pedersen, Birgitte Hansen, Torben Sigsgaard, Jørn Olsen, Jörg Schullehner, Marie Pedersen, Leslie T Stayner
Evidence is emerging that preterm birth (PTB, birth before 37 completed weeks of gestation), a risk factor for neonatal mortality and future morbidity, may be induced by maternal nitrate ( ) exposure from drinking water. The objective of this study is to assess the association between maternal exposure to nitrate and the risk of PTB in a nationwide study of liveborn singletons.
Methods: We estimated maternal nitrate exposure from household tap water for 1,055,584 births in Denmark to Danish-born parents during 1991-2015 by linkage of individual home address(es) with nitrate concentrations from a national monitoring database. Nitrate exposure during pregnancy was modeled using four categories and continuously. Logistic models adjusted for sex, birth year, birth order, urbanicity, and maternal age, smoking, education, income, and employment, with generalized estimating equations were used to account for sibling clusters.
Results: A total of 1,009,189 births were included, comprising 51,747 PTB. An increase in the risk of PTB was seen across categories of exposure (P < 0.001) with an odds ratio (OR) in the uppermost category (>25 mg/L nitrate) of 1.05 (95% confidence interval [CI] = 1.00, 1.10). Evidence of an exposure-response relationship was observed in models using continuous nitrate (OR = 1.01 [95% CI = 1.00, 1.03] per 10 mg/L nitrate). In sensitivity analyses, results were robust to the addition of variables for short inter-pregnancy interval (<1 year between births), maternal pre-pregnancy body mass index, paternal socioeconomic status and age, season of birth, and inclusion of post-term births. Results were virtually unchanged when the analysis was restricted to women exposed to less than the current European Union standard of 50 mg/L.
Conclusion: We observed an increasing risk of PTB with increases in nitrate in household tap water. These findings add to a growing body of evidence of adverse effects from nitrate in drinking water at levels below current regulatory levels.
{"title":"Prenatal exposure to nitrate from drinking water and the risk of preterm birth: A Danish nationwide cohort study.","authors":"Vanessa R Coffman, Anja Søndergaard Jensen, Betina B Trabjerg, Carsten Bøcker Pedersen, Birgitte Hansen, Torben Sigsgaard, Jørn Olsen, Jörg Schullehner, Marie Pedersen, Leslie T Stayner","doi":"10.1097/EE9.0000000000000223","DOIUrl":"10.1097/EE9.0000000000000223","url":null,"abstract":"<p><p>Evidence is emerging that preterm birth (PTB, birth before 37 completed weeks of gestation), a risk factor for neonatal mortality and future morbidity, may be induced by maternal nitrate ( <math> <mstyle> <msubsup><mrow><mi>N</mi> <mi>O</mi></mrow> <mrow><mn>3</mn></mrow> <mrow><mo>-</mo></mrow> </msubsup> </mstyle> </math> ) exposure from drinking water. The objective of this study is to assess the association between maternal exposure to nitrate and the risk of PTB in a nationwide study of liveborn singletons.</p><p><strong>Methods: </strong>We estimated maternal nitrate exposure from household tap water for 1,055,584 births in Denmark to Danish-born parents during 1991-2015 by linkage of individual home address(es) with nitrate concentrations from a national monitoring database. Nitrate exposure during pregnancy was modeled using four categories and continuously. Logistic models adjusted for sex, birth year, birth order, urbanicity, and maternal age, smoking, education, income, and employment, with generalized estimating equations were used to account for sibling clusters.</p><p><strong>Results: </strong>A total of 1,009,189 births were included, comprising 51,747 PTB. An increase in the risk of PTB was seen across categories of exposure (<i>P</i> < 0.001) with an odds ratio (OR) in the uppermost category (>25 mg/L nitrate) of 1.05 (95% confidence interval [CI] = 1.00, 1.10). Evidence of an exposure-response relationship was observed in models using continuous nitrate (OR = 1.01 [95% CI = 1.00, 1.03] per 10 mg/L nitrate). In sensitivity analyses, results were robust to the addition of variables for short inter-pregnancy interval (<1 year between births), maternal pre-pregnancy body mass index, paternal socioeconomic status and age, season of birth, and inclusion of post-term births. Results were virtually unchanged when the analysis was restricted to women exposed to less than the current European Union standard of 50 mg/L.</p><p><strong>Conclusion: </strong>We observed an increasing risk of PTB with increases in nitrate in household tap water. These findings add to a growing body of evidence of adverse effects from nitrate in drinking water at levels below current regulatory levels.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":" ","pages":"e223"},"PeriodicalIF":3.8,"publicationDate":"2022-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/f3/cc/ee9-6-e223.PMC9556052.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33516648","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}
Pub Date : 2022-07-19eCollection Date: 2022-08-01DOI: 10.1097/EE9.0000000000000219
Leslie Michele-Ange Kouam Youogo, Marie-Elise Parent, Perry Hystad, Paul J Villeneuve
Ambient air pollution is a human carcinogen and a possible risk factor for prostate cancer.
Methods: We investigated associations between ambient concentrations particulate matter 2.5 (PM2.5) and nitrogen dioxide (NO2) and incident prostate cancer in a Canadian case-control study. Between 1994 and 1997, cases were identified from provincial cancer registries, and a population-based series of controls was recruited. Among men 50 years of age or older, risk factor and residential history data (1975 to 1994) were collected from 1,420 prostate cancer cases and 1,424 controls. Three methods were used to estimate the residential mean exposure to PM2.5 and NO2 during this period: (1) satellite-derived observations; (2) satellite-derived observations scaled with historical fixed-site measurements; and (3) a national land-use regression (LUR) model. Odds ratios (ORs) and their 95% confidence intervals (CIs) in relation to interquartile range (IQR) increases in PM2.5 and NO2 were estimated using logistic regression, adjusting for personal and contextual factors.
Results: We found positive associations between exposure to PM2.5 and NO2 over the previous 20 years and prostate cancer. An IQR increase in PM2.5 (3.56 µg/m3 for satellite and 4.48 µg/m3 for scaled satellite observations) yielded ORs of 1.28 (95% CI = 1.07, 1.52) and 1.20 (95% CI = 1.03, 1.40), respectively. For NO2, IQR increases (1.45 ppb for satellite, 15.18 ppb for scaled satellite-derived information, and 15.39 ppb for the national LUR) were associated with ORs of 1.09 (95% CI = 0.95, 1.24), 1.21 (95% CI = 1.02, 1.43), and 1.19 (95% CI = 1.03, 1.38), respectively.
Conclusions: Our findings support the hypothesis that ambient air pollution increases the risk of prostate cancer.
环境空气污染是一种人类致癌物,也是前列腺癌的可能危险因素。方法:我们在加拿大的一项病例对照研究中调查了环境颗粒物2.5 (PM2.5)和二氧化氮(NO2)浓度与前列腺癌发病率的关系。在1994年至1997年期间,从省级癌症登记处确定病例,并招募了基于人群的一系列对照。在50岁或以上的男性中,收集了1420例前列腺癌病例和1424例对照的风险因素和居住史数据(1975年至1994年)。利用3种方法估算了这一时期居民PM2.5和NO2的平均暴露量:(1)卫星观测;(2)基于历史固定地点测量的卫星观测数据;(3)国家土地利用回归(LUR)模型。在调整个人和环境因素后,使用逻辑回归估计PM2.5和NO2的比值比(ORs)及其与四分位数范围(IQR)增加相关的95%置信区间(ci)。结果:我们发现在过去20年中暴露于PM2.5和二氧化氮与前列腺癌之间存在正相关。PM2.5的IQR增加(卫星观测值为3.56µg/m3,缩放卫星观测值为4.48µg/m3)分别产生1.28 (95% CI = 1.07, 1.52)和1.20 (95% CI = 1.03, 1.40)。对于NO2, IQR增加(卫星1.45 ppb,卫星衍生信息15.18 ppb,国家LUR 15.39 ppb)的or分别为1.09 (95% CI = 0.95, 1.24), 1.21 (95% CI = 1.02, 1.43)和1.19 (95% CI = 1.03, 1.38)。结论:我们的研究结果支持了环境空气污染增加前列腺癌风险的假设。
{"title":"Ambient air pollution and prostate cancer risk in a population-based Canadian case-control study.","authors":"Leslie Michele-Ange Kouam Youogo, Marie-Elise Parent, Perry Hystad, Paul J Villeneuve","doi":"10.1097/EE9.0000000000000219","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000219","url":null,"abstract":"<p><p>Ambient air pollution is a human carcinogen and a possible risk factor for prostate cancer.</p><p><strong>Methods: </strong>We investigated associations between ambient concentrations particulate matter 2.5 (PM<sub>2.5</sub>) and nitrogen dioxide (NO<sub>2</sub>) and incident prostate cancer in a Canadian case-control study. Between 1994 and 1997, cases were identified from provincial cancer registries, and a population-based series of controls was recruited. Among men 50 years of age or older, risk factor and residential history data (1975 to 1994) were collected from 1,420 prostate cancer cases and 1,424 controls. Three methods were used to estimate the residential mean exposure to PM<sub>2.5</sub> and NO<sub>2</sub> during this period: (1) satellite-derived observations; (2) satellite-derived observations scaled with historical fixed-site measurements; and (3) a national land-use regression (LUR) model. Odds ratios (ORs) and their 95% confidence intervals (CIs) in relation to interquartile range (IQR) increases in PM<sub>2.5</sub> and NO<sub>2</sub> were estimated using logistic regression, adjusting for personal and contextual factors.</p><p><strong>Results: </strong>We found positive associations between exposure to PM<sub>2.5</sub> and NO<sub>2</sub> over the previous 20 years and prostate cancer. An IQR increase in PM<sub>2.5</sub> (3.56 µg/m<sup>3</sup> for satellite and 4.48 µg/m<sup>3</sup> for scaled satellite observations) yielded ORs of 1.28 (95% CI = 1.07, 1.52) and 1.20 (95% CI = 1.03, 1.40), respectively. For NO<sub>2</sub>, IQR increases (1.45 ppb for satellite, 15.18 ppb for scaled satellite-derived information, and 15.39 ppb for the national LUR) were associated with ORs of 1.09 (95% CI = 0.95, 1.24), 1.21 (95% CI = 1.02, 1.43), and 1.19 (95% CI = 1.03, 1.38), respectively.</p><p><strong>Conclusions: </strong>Our findings support the hypothesis that ambient air pollution increases the risk of prostate cancer.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":" ","pages":"e219"},"PeriodicalIF":3.6,"publicationDate":"2022-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9374191/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40633126","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}
Pub Date : 2022-06-29eCollection Date: 2022-08-01DOI: 10.1097/EE9.0000000000000218
Tara P McAlexander, Jyotsna S Jagai, Leslie A McClure
The prevalence of type 2 diabetes (T2D) has increased in the United States, and recent studies suggest that environmental factors contribute to T2D risk. We sought to understand if environmental factors were associated with the rate and magnitude of increase in diabetes prevalence at the county level.
Methods: We obtained age-adjusted diabetes prevalence estimates from the CDC for 3,137 US counties from 2004 to 2017. We applied latent growth mixture models to these data to identify classes of counties with similar trends in diabetes prevalence over time, stratified by Rural Urban Continuum Codes (RUCC). We then compared mean values of the US EPA Environmental Quality Index (EQI) 2006-2010, overall and for each of the five domain indices (air, water, land, sociodemographic, and built), with RUCC-specific latent class to examine associations of environmental factors and class of diabetes prevalence trajectory.
Results: Overall diabetes prevalence trends between 2004 and 2017 were similar across all RUCC strata. We identified two classes among metropolitan urbanized (RUCC 1) counties; four classes among non-metro urbanized (RUCC 2) counties; and three classes among less urbanized (RUCC 3) and thinly populated (RUCC 4) counties. Associations with overall EQI values and class of diabetes prevalence trends differed by RUCC strata, with the clearest association between poor air EQI and steeper increases in diabetes prevalence among rural counties (RUCC 3 and 4).
Conclusions: Similarities in county-level diabetes prevalence trends between 2004 and 2017 were identified for each RUCC strata, although associations with environmental factors varied by rurality.
{"title":"Latent growth trajectories of county-level diabetes prevalence in the United States, 2004-2017, and associations with overall environmental quality.","authors":"Tara P McAlexander, Jyotsna S Jagai, Leslie A McClure","doi":"10.1097/EE9.0000000000000218","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000218","url":null,"abstract":"<p><p>The prevalence of type 2 diabetes (T2D) has increased in the United States, and recent studies suggest that environmental factors contribute to T2D risk. We sought to understand if environmental factors were associated with the rate and magnitude of increase in diabetes prevalence at the county level.</p><p><strong>Methods: </strong>We obtained age-adjusted diabetes prevalence estimates from the CDC for 3,137 US counties from 2004 to 2017. We applied latent growth mixture models to these data to identify classes of counties with similar trends in diabetes prevalence over time, stratified by Rural Urban Continuum Codes (RUCC). We then compared mean values of the US EPA Environmental Quality Index (EQI) 2006-2010, overall and for each of the five domain indices (air, water, land, sociodemographic, and built), with RUCC-specific latent class to examine associations of environmental factors and class of diabetes prevalence trajectory.</p><p><strong>Results: </strong>Overall diabetes prevalence trends between 2004 and 2017 were similar across all RUCC strata. We identified two classes among metropolitan urbanized (RUCC 1) counties; four classes among non-metro urbanized (RUCC 2) counties; and three classes among less urbanized (RUCC 3) and thinly populated (RUCC 4) counties. Associations with overall EQI values and class of diabetes prevalence trends differed by RUCC strata, with the clearest association between poor air EQI and steeper increases in diabetes prevalence among rural counties (RUCC 3 and 4).</p><p><strong>Conclusions: </strong>Similarities in county-level diabetes prevalence trends between 2004 and 2017 were identified for each RUCC strata, although associations with environmental factors varied by rurality.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":" ","pages":"e218"},"PeriodicalIF":3.6,"publicationDate":"2022-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/8b/fb/ee9-6-e218.PMC9374184.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40633127","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}
Pub Date : 2022-06-01DOI: 10.1097/EE9.0000000000000212
J. Laiho, O. Laitinen, Johannes Malkamäki, L. Puustinen, A. Sinkkonen, J. Pärkkä, H. Hyöty
The incidence of immune-mediated diseases (IMDs) is increasing rapidly in the developed countries constituting a huge medical, economic, and societal challenge. The exposome plays an important role since genetic factors cannot explain such a rapid change. In the Human Exposomic Determinants of Immune Mediated Diseases (HEDIMED) project, altogether 22 academic and industrial partners join their multidisciplinary forces to identify exposomic determinants that are driving the IMD epidemic. The project is based on a combination of data and biological samples from large clinical cohorts constituting about 350,000 pregnant women, 30,000 children prospectively followed from birth, and 7,000 children from cross-sectional studies. HEDIMED focuses on common chronic IMDs that cause a significant disease burden, including type 1 diabetes, celiac disease, allergy, and asthma. Exposomic disease determinants and the underlying biological pathways will be identified by an exploratory approach using advanced omics and multiplex technologies combined with cutting-edge data mining technologies. Emphasis is put on fetal and childhood exposome since the IMD disease processes start early. Inclusion of several IMDs makes it possible to identify common exposomic determinants for the diseases, thus facilitating the development of widely operating preventive and curative treatments. HEDIMED includes data and samples from birth cohorts and clinical trials that have used exposomic interventions and cell and organ culture models to identify mechanisms of the observed associations. Importantly, HEDIMED generates a toolbox that offers science-based functional tools for key stakeholders to control the IMD epidemic. Altogether, HEDIMED aims at innovations, which become widely exploited in diagnostic, therapeutic, preventive, and health economic approaches.
{"title":"Exposomic determinants of immune-mediated diseases","authors":"J. Laiho, O. Laitinen, Johannes Malkamäki, L. Puustinen, A. Sinkkonen, J. Pärkkä, H. Hyöty","doi":"10.1097/EE9.0000000000000212","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000212","url":null,"abstract":"The incidence of immune-mediated diseases (IMDs) is increasing rapidly in the developed countries constituting a huge medical, economic, and societal challenge. The exposome plays an important role since genetic factors cannot explain such a rapid change. In the Human Exposomic Determinants of Immune Mediated Diseases (HEDIMED) project, altogether 22 academic and industrial partners join their multidisciplinary forces to identify exposomic determinants that are driving the IMD epidemic. The project is based on a combination of data and biological samples from large clinical cohorts constituting about 350,000 pregnant women, 30,000 children prospectively followed from birth, and 7,000 children from cross-sectional studies. HEDIMED focuses on common chronic IMDs that cause a significant disease burden, including type 1 diabetes, celiac disease, allergy, and asthma. Exposomic disease determinants and the underlying biological pathways will be identified by an exploratory approach using advanced omics and multiplex technologies combined with cutting-edge data mining technologies. Emphasis is put on fetal and childhood exposome since the IMD disease processes start early. Inclusion of several IMDs makes it possible to identify common exposomic determinants for the diseases, thus facilitating the development of widely operating preventive and curative treatments. HEDIMED includes data and samples from birth cohorts and clinical trials that have used exposomic interventions and cell and organ culture models to identify mechanisms of the observed associations. Importantly, HEDIMED generates a toolbox that offers science-based functional tools for key stakeholders to control the IMD epidemic. Altogether, HEDIMED aims at innovations, which become widely exploited in diagnostic, therapeutic, preventive, and health economic approaches.","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46090956","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}
Pub Date : 2022-06-01DOI: 10.1097/EE9.0000000000000213
P. Jain, Amit Kapoor, P. Rubeshkumar, Mohankumar Raju, Bency Joseph, P. Bhat, P. Ganeshkumar, C. Kesavachandran, D. Patel, N. Manickam, P. Kaur
Background: Chemical leakages cause devastating health effects on humans. On 6 February 2020, seven deaths were reported following a hazardous chemical leakage in a village in Uttar Pradesh, India. We investigated the event to identify the cause and propose recommendations. Methods: We defined a case as sudden onset of breathlessness, headache, or death in the village, 6–7 February 2020. We conducted a house-to-house case search and calculated attack rate (AR) and case-fatality rate (CFR) by age and gender. We conducted an environmental investigation at the leakage site and sent the chemicals for forensic analysis. We obtained the cause of death through autopsy reports. Results: Out of 2,942 residents, we identified 23 cases (AR = 8/1,000) and seven deaths (CFR = 30%). The median age of the case was 42 years (range, 2–64 years). The AR was higher among males (14/1,000 [19/1,402]). All the 23 case-patients who were sleeping at the chemical leakage site or visited to witness the event developed symptoms, and all seven cases who were sleeping within 150 meters of the leakage site died. The environmental investigation revealed leakage of hazardous substances from the storage tank. Toxicology analysis confirmed the leaked chemical as Lindane (gamma-hexachlorocyclohexane), and autopsy reports confirmed the cause of death as asphyxia. Conclusions: Asphyxia following the leakage of Lindane from the storage tank possibly led to sudden deaths. We recommend using leak-proof tanks to ensure safe storage and disposal, law enforcement, and regulations to prevent people from staying close to chemical storage sites.
{"title":"Sudden deaths due to accidental leakage of Lindane from a storage tank in a village, Sitapur, Uttar Pradesh, India, 2020","authors":"P. Jain, Amit Kapoor, P. Rubeshkumar, Mohankumar Raju, Bency Joseph, P. Bhat, P. Ganeshkumar, C. Kesavachandran, D. Patel, N. Manickam, P. Kaur","doi":"10.1097/EE9.0000000000000213","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000213","url":null,"abstract":"Background: Chemical leakages cause devastating health effects on humans. On 6 February 2020, seven deaths were reported following a hazardous chemical leakage in a village in Uttar Pradesh, India. We investigated the event to identify the cause and propose recommendations. Methods: We defined a case as sudden onset of breathlessness, headache, or death in the village, 6–7 February 2020. We conducted a house-to-house case search and calculated attack rate (AR) and case-fatality rate (CFR) by age and gender. We conducted an environmental investigation at the leakage site and sent the chemicals for forensic analysis. We obtained the cause of death through autopsy reports. Results: Out of 2,942 residents, we identified 23 cases (AR = 8/1,000) and seven deaths (CFR = 30%). The median age of the case was 42 years (range, 2–64 years). The AR was higher among males (14/1,000 [19/1,402]). All the 23 case-patients who were sleeping at the chemical leakage site or visited to witness the event developed symptoms, and all seven cases who were sleeping within 150 meters of the leakage site died. The environmental investigation revealed leakage of hazardous substances from the storage tank. Toxicology analysis confirmed the leaked chemical as Lindane (gamma-hexachlorocyclohexane), and autopsy reports confirmed the cause of death as asphyxia. Conclusions: Asphyxia following the leakage of Lindane from the storage tank possibly led to sudden deaths. We recommend using leak-proof tanks to ensure safe storage and disposal, law enforcement, and regulations to prevent people from staying close to chemical storage sites.","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48017334","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}
Pub Date : 2022-04-22eCollection Date: 2022-06-01DOI: 10.1097/EE9.0000000000000201
Elena Colicino, Katerina Margetaki, Damaskini Valvi, Nicolo Foppa Pedretti, Nikos Stratakis, Marina Vafeiadi, Theano Roumeliotaki, Soterios A Kyrtopoulos, Hannu Kiviranta, Euripides G Stephanou, Manolis Kogevinas, Rob McConnell, Kiros T Berhane, Leda Chatzi, David V Conti
Background: Prenatal exposure to organochlorine compounds (OCs) has been associated with increased childhood body mass index (BMI); however, only a few studies have focused on longitudinal BMI trajectories, and none of them used multiple exposure mixture approaches.
Aim: To determine the association between in-utero exposure to eight OCs and childhood BMI measures (BMI and BMI z-score) at 4 years and their yearly change across 4-12 years of age in 279 Rhea child-mother dyads.
Methods: We applied three approaches: (1) linear mixed-effect regressions (LMR) to associate individual compounds with BMI measures; (2) Bayesian weighted quantile sum regressions (BWQSR) to provide an overall OC mixture association with BMI measures; and (3)Bayesian varying coefficient kernel machine regressions (BVCKMR) to model nonlinear and nonadditive associations.
Results: In the LMR, yearly change of BMI measures was consistently associated with a quartile increase in hexachlorobenzene (HCB) (estimate [95% Confidence or Credible interval] BMI: 0.10 [0.06, 0.14]; BMI z-score: 0.02 [0.01, 0.04]). BWQSR results showed that a quartile increase in mixture concentrations was associated with yearly increase of BMI measures (BMI: 0.10 [0.01, 0.18]; BMI z-score: 0.03 [0.003, 0.06]). In the BVCKMR, a quartile increase in dichlorodiphenyldichloroethylene concentrations was associated with higher BMI measures at 4 years (BMI: 0.33 [0.24, 0.43]; BMI z-score: 0.19 [0.15, 0.24]); whereas a quartile increase in HCB and polychlorinated biphenyls (PCB)-118 levels was positively associated with BMI measures yearly change (BMI: HCB:0.10 [0.07, 0.13], PCB-118:0.08 [0.04, 012]; BMI z-score: HCB:0.03 [0.02, 0.05], PCB-118:0.02 [0.002,04]). BVCKMR suggested that PCBs had nonlinear relationships with BMI measures, and HCB interacted with other compounds.
Conclusions: All analyses consistently demonstrated detrimental associations between prenatal OC exposures and childhood BMI measures.
{"title":"Prenatal exposure to multiple organochlorine compounds and childhood body mass index.","authors":"Elena Colicino, Katerina Margetaki, Damaskini Valvi, Nicolo Foppa Pedretti, Nikos Stratakis, Marina Vafeiadi, Theano Roumeliotaki, Soterios A Kyrtopoulos, Hannu Kiviranta, Euripides G Stephanou, Manolis Kogevinas, Rob McConnell, Kiros T Berhane, Leda Chatzi, David V Conti","doi":"10.1097/EE9.0000000000000201","DOIUrl":"10.1097/EE9.0000000000000201","url":null,"abstract":"<p><strong>Background: </strong>Prenatal exposure to organochlorine compounds (OCs) has been associated with increased childhood body mass index (BMI); however, only a few studies have focused on longitudinal BMI trajectories, and none of them used multiple exposure mixture approaches.</p><p><strong>Aim: </strong>To determine the association between <i>in-utero</i> exposure to eight OCs and childhood BMI measures (BMI and BMI z-score) at 4 years and their yearly change across 4-12 years of age in 279 Rhea child-mother dyads.</p><p><strong>Methods: </strong>We applied three approaches: (1) linear mixed-effect regressions (LMR) to associate individual compounds with BMI measures; (2) Bayesian weighted quantile sum regressions (BWQSR) to provide an overall OC mixture association with BMI measures; and (3)Bayesian varying coefficient kernel machine regressions (BVCKMR) to model nonlinear and nonadditive associations.</p><p><strong>Results: </strong>In the LMR, yearly change of BMI measures was consistently associated with a quartile increase in hexachlorobenzene (HCB) (estimate [95% Confidence or Credible interval] BMI: 0.10 [0.06, 0.14]; BMI z-score: 0.02 [0.01, 0.04]). BWQSR results showed that a quartile increase in mixture concentrations was associated with yearly increase of BMI measures (BMI: 0.10 [0.01, 0.18]; BMI z-score: 0.03 [0.003, 0.06]). In the BVCKMR, a quartile increase in dichlorodiphenyldichloroethylene concentrations was associated with higher BMI measures at 4 years (BMI: 0.33 [0.24, 0.43]; BMI z-score: 0.19 [0.15, 0.24]); whereas a quartile increase in HCB and polychlorinated biphenyls (PCB)-118 levels was positively associated with BMI measures yearly change (BMI: HCB:0.10 [0.07, 0.13], PCB-118:0.08 [0.04, 012]; BMI z-score: HCB:0.03 [0.02, 0.05], PCB-118:0.02 [0.002,04]). BVCKMR suggested that PCBs had nonlinear relationships with BMI measures, and HCB interacted with other compounds.</p><p><strong>Conclusions: </strong>All analyses consistently demonstrated detrimental associations between prenatal OC exposures and childhood BMI measures.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"66 3","pages":"e201"},"PeriodicalIF":3.3,"publicationDate":"2022-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9187184/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41304130","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}