Pub Date : 2024-03-28DOI: 10.1097/ee9.0000000000000305
H. Laue, B. Lanphear, A.M. Calafat, Kim M. Cecil, Aimin Chen, Yingying Xu, Heidi J. Kalkwarf, J. C. Madan, M. R. Karagas, K. Yolton, A. Fleisch, Joseph M. Braun
Triclosan is an endocrine-disrupting chemical, but associations with pubertal outcomes remain unclear. We examined associations of gestational and childhood triclosan with adolescent hormone concentrations and pubertal stage. We quantified urinary triclosan concentrations twice during pregnancy and seven times between birth and 12 years in participants recruited from Cincinnati, OH (2003–2006). We averaged concentrations across pregnancy and childhood and separately considered individual exposure periods in multiple informant models. At 12 years, we measured serum hormone concentrations (males [n = 72] and females [n = 84]—dehydroepiandrosterone-sulfate, luteinizing hormone, follicle-stimulating hormone; males—testosterone; females—estradiol). Also at age 12 years, participants self-reported physical development and menarchal timing. We estimated associations (95% confidence interval) of triclosan with hormone concentrations, more advanced physical development, and age at menarche. For females, each doubling of childhood triclosan was associated with 16% lower estradiol concentrations (−29%, 0%), with stronger associations for measures closer to adolescence. We found suggestive evidence that higher triclosan at any age was associated with ~10% (for gestational triclosan: −18%, −2%) lower follicle-stimulating hormone concentrations among males and early postnatal (1–3 years) triclosan was associated with 63% (5%, 96%) lower odds of advanced pubic hair development in females. In multiple informant models, each doubling of gestational triclosan concentrations was associated with 5% (0%, 9%) earlier age at menarche, equivalent to 5.5 months. Gestational and childhood triclosan concentrations were related to some pubertal outcomes including hormone concentrations and age at menarche. Our findings highlight the relevance of elucidating potential sex-specific and time-dependent actions of triclosan.
{"title":"Time-varying associations of gestational and childhood triclosan with pubertal and adrenarchal outcomes in early adolescence","authors":"H. Laue, B. Lanphear, A.M. Calafat, Kim M. Cecil, Aimin Chen, Yingying Xu, Heidi J. Kalkwarf, J. C. Madan, M. R. Karagas, K. Yolton, A. Fleisch, Joseph M. Braun","doi":"10.1097/ee9.0000000000000305","DOIUrl":"https://doi.org/10.1097/ee9.0000000000000305","url":null,"abstract":"\u0000 \u0000 Triclosan is an endocrine-disrupting chemical, but associations with pubertal outcomes remain unclear. We examined associations of gestational and childhood triclosan with adolescent hormone concentrations and pubertal stage.\u0000 \u0000 \u0000 \u0000 We quantified urinary triclosan concentrations twice during pregnancy and seven times between birth and 12 years in participants recruited from Cincinnati, OH (2003–2006). We averaged concentrations across pregnancy and childhood and separately considered individual exposure periods in multiple informant models. At 12 years, we measured serum hormone concentrations (males [n = 72] and females [n = 84]—dehydroepiandrosterone-sulfate, luteinizing hormone, follicle-stimulating hormone; males—testosterone; females—estradiol). Also at age 12 years, participants self-reported physical development and menarchal timing. We estimated associations (95% confidence interval) of triclosan with hormone concentrations, more advanced physical development, and age at menarche.\u0000 \u0000 \u0000 \u0000 For females, each doubling of childhood triclosan was associated with 16% lower estradiol concentrations (−29%, 0%), with stronger associations for measures closer to adolescence. We found suggestive evidence that higher triclosan at any age was associated with ~10% (for gestational triclosan: −18%, −2%) lower follicle-stimulating hormone concentrations among males and early postnatal (1–3 years) triclosan was associated with 63% (5%, 96%) lower odds of advanced pubic hair development in females. In multiple informant models, each doubling of gestational triclosan concentrations was associated with 5% (0%, 9%) earlier age at menarche, equivalent to 5.5 months.\u0000 \u0000 \u0000 \u0000 Gestational and childhood triclosan concentrations were related to some pubertal outcomes including hormone concentrations and age at menarche. Our findings highlight the relevance of elucidating potential sex-specific and time-dependent actions of triclosan.\u0000","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140372687","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 : 2024-03-18DOI: 10.1097/ee9.0000000000000300
Jeremy M. Schraw, Kara E. Rudolph, Charles J. Shumate, M. Gribble
Direct potable reuse (DPR) involves adding purified wastewater that has not passed through an environmental buffer into a water distribution system. DPR may help address water shortages and is approved or is under consideration as a source of drinking water for several water-stressed population centers in the United States, however, there are no studies of health outcomes in populations who receive DPR drinking water. Our objective was to determine whether the introduction of DPR for certain public water systems in Texas was associated with changes in birth defect prevalence. We obtained data on maternal characteristics for all live births and birth defects cases regardless of pregnancy outcome in Texas from 2003 to 2017 from the Texas Birth Defects Registry and birth and fetal death records. The ridge augmented synthetic control method was used to model changes in birth defect prevalence (per 10,000 live births) following the adoption of DPR by four Texas counties in mid-2013, with county-level data on maternal age, percent women without a high school diploma, percent who identified as Hispanic/Latina or non-Hispanic/Latina Black, and rural-urban continuum code as covariates. There were nonstatistically significant increases in prevalence of all birth defects collectively (average treatment effect in the treated = 53.6) and congenital heart disease (average treatment effect in the treated = 287.3) since June 2013. The estimated prevalence of neural tube defects was unchanged. We estimated nonstatistically significant increases in birth defect prevalence following the implementation of DPR in four West Texas counties. Further research is warranted to inform water policy decisions.
{"title":"Direct potable reuse and birth defects prevalence in Texas: An augmented synthetic control method analysis of data from a population-based birth defects registry","authors":"Jeremy M. Schraw, Kara E. Rudolph, Charles J. Shumate, M. Gribble","doi":"10.1097/ee9.0000000000000300","DOIUrl":"https://doi.org/10.1097/ee9.0000000000000300","url":null,"abstract":"\u0000 \u0000 Direct potable reuse (DPR) involves adding purified wastewater that has not passed through an environmental buffer into a water distribution system. DPR may help address water shortages and is approved or is under consideration as a source of drinking water for several water-stressed population centers in the United States, however, there are no studies of health outcomes in populations who receive DPR drinking water. Our objective was to determine whether the introduction of DPR for certain public water systems in Texas was associated with changes in birth defect prevalence.\u0000 \u0000 \u0000 \u0000 We obtained data on maternal characteristics for all live births and birth defects cases regardless of pregnancy outcome in Texas from 2003 to 2017 from the Texas Birth Defects Registry and birth and fetal death records. The ridge augmented synthetic control method was used to model changes in birth defect prevalence (per 10,000 live births) following the adoption of DPR by four Texas counties in mid-2013, with county-level data on maternal age, percent women without a high school diploma, percent who identified as Hispanic/Latina or non-Hispanic/Latina Black, and rural-urban continuum code as covariates.\u0000 \u0000 \u0000 \u0000 There were nonstatistically significant increases in prevalence of all birth defects collectively (average treatment effect in the treated = 53.6) and congenital heart disease (average treatment effect in the treated = 287.3) since June 2013. The estimated prevalence of neural tube defects was unchanged.\u0000 \u0000 \u0000 \u0000 We estimated nonstatistically significant increases in birth defect prevalence following the implementation of DPR in four West Texas counties. Further research is warranted to inform water policy decisions.\u0000","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140231842","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 : 2024-03-14DOI: 10.1097/ee9.0000000000000303
Rudra K. Shrestha, Ioana Sevcenco, Priscila Casari, Henry Ngo, Anders Erickson, Martin Lavoie, Deena Hinshaw, Bonnie Henry, Xibiao Ye
Studies show that more than 5.1 million deaths annually are attributed to nonoptimal temperatures, including extreme cold and extreme heat. However, those studies mostly report average estimates across large geographical areas. The health risks attributed to nonoptimal temperatures in British Columbia (BC) are reported incompletely or limit the study area to urban centers. In this study, we aim to estimate the attributable deaths linked to nonoptimal temperatures in all five regional health authorities (RHAs) of BC from 2001 to 2021. We applied the widely used distributed lag nonlinear modeling approach to estimate temperature–mortality association in the RHAs of BC, using daily all-cause deaths and 1 × 1 km gridded daily mean temperature. We evaluated the model by comparing the model-estimated attributable number of deaths during the 2021 heat dome to the number of heat-related deaths confirmed by the British Columbia Coroners Service. Overall, between 2001 and 2021, we estimate that 7.17% (95% empirical confidence interval = 3.15, 10.32) of deaths in BC were attributed to nonoptimal temperatures, the majority of which are attributed to cold. On average, the mortality rates attributable to moderate cold, moderate heat, extreme cold, and extreme heat were 47.04 (95% confidence interval [CI] = 45.83, 48.26), 0.94 (95% CI = 0.81, 1.08), 2.88 (95% CI = 2.05, 3.71), and 3.10 (95% CI = 1.79, 4.4) per 100,000 population per year, respectively. Our results show significant spatial variability in deaths attributable to nonoptimal temperatures across BC. We find that the effect of extreme temperatures is significantly less compared to milder nonoptimal temperatures between 2001 and 2021. However, the increased contribution of extreme heat cannot be ruled out in the near future.
{"title":"Estimating the impacts of nonoptimal temperatures on mortality: A study in British Columbia, Canada, 2001–2021","authors":"Rudra K. Shrestha, Ioana Sevcenco, Priscila Casari, Henry Ngo, Anders Erickson, Martin Lavoie, Deena Hinshaw, Bonnie Henry, Xibiao Ye","doi":"10.1097/ee9.0000000000000303","DOIUrl":"https://doi.org/10.1097/ee9.0000000000000303","url":null,"abstract":"\u0000 \u0000 Studies show that more than 5.1 million deaths annually are attributed to nonoptimal temperatures, including extreme cold and extreme heat. However, those studies mostly report average estimates across large geographical areas. The health risks attributed to nonoptimal temperatures in British Columbia (BC) are reported incompletely or limit the study area to urban centers. In this study, we aim to estimate the attributable deaths linked to nonoptimal temperatures in all five regional health authorities (RHAs) of BC from 2001 to 2021.\u0000 \u0000 \u0000 \u0000 We applied the widely used distributed lag nonlinear modeling approach to estimate temperature–mortality association in the RHAs of BC, using daily all-cause deaths and 1 × 1 km gridded daily mean temperature. We evaluated the model by comparing the model-estimated attributable number of deaths during the 2021 heat dome to the number of heat-related deaths confirmed by the British Columbia Coroners Service.\u0000 \u0000 \u0000 \u0000 Overall, between 2001 and 2021, we estimate that 7.17% (95% empirical confidence interval = 3.15, 10.32) of deaths in BC were attributed to nonoptimal temperatures, the majority of which are attributed to cold. On average, the mortality rates attributable to moderate cold, moderate heat, extreme cold, and extreme heat were 47.04 (95% confidence interval [CI] = 45.83, 48.26), 0.94 (95% CI = 0.81, 1.08), 2.88 (95% CI = 2.05, 3.71), and 3.10 (95% CI = 1.79, 4.4) per 100,000 population per year, respectively.\u0000 \u0000 \u0000 \u0000 Our results show significant spatial variability in deaths attributable to nonoptimal temperatures across BC. We find that the effect of extreme temperatures is significantly less compared to milder nonoptimal temperatures between 2001 and 2021. However, the increased contribution of extreme heat cannot be ruled out in the near future.\u0000","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140243777","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 : 2024-03-13DOI: 10.1097/ee9.0000000000000304
G. Christensen, Metrecia L. Terrell, Brad D. Pearce, Robert B. Hood, Hillary Barton, Melanie Pearson, Michele Marcus
Although the causes of attention-deficit/hyperactivity disorder (ADHD) and autism have not been identified, exposure to endocrine-disrupting chemicals, such as polybrominated biphenyl (PBB), during fetal development and early life has been suspected to impact neurological development. This study aims to investigate the association between prenatal and early life exposure to PBB and the development of ADHD and autism later in life. Data from the Michigan PBB Registry, a cohort of Michigan residents who had been exposed to PBB in a mass contamination event in 1973, was leveraged for this nested case-control analysis among two distinct samples: (1) Those who self-reported ADHD or autism diagnosis, and (2) mothers who reported their child’s ADHD or autism diagnosis. PBB exposure was measured in participants of the PBB Registry, and the mother’s PBB level was used in mother-reported analyses. Cases were matched with controls by sex and year of birth. Conditional logistic regression models were used to estimate the association between PBB level and case status. PBB levels were higher among those who were exposed in early life compared with those exposed in utero (geometric mean: 0.300 ng/ml vs. 0.016 ng/ml). Among women in this cohort, a higher than expected proportion of self-reported ADHD diagnosis (11.11%), compared with population estimates. PBB was not associated with ADHD or autism in either self-reported or mother-reported analyses. This study adds to the sparse literature about prenatal and early life exposure to PBB-153 and ADHD and autism. Future studies should examine potential effect modification by sex.
{"title":"Exploring autism spectrum disorder (ASD) and attention deficit disorder (ADD/ADHD) in children exposed to polybrominated biphenyl","authors":"G. Christensen, Metrecia L. Terrell, Brad D. Pearce, Robert B. Hood, Hillary Barton, Melanie Pearson, Michele Marcus","doi":"10.1097/ee9.0000000000000304","DOIUrl":"https://doi.org/10.1097/ee9.0000000000000304","url":null,"abstract":"\u0000 \u0000 Although the causes of attention-deficit/hyperactivity disorder (ADHD) and autism have not been identified, exposure to endocrine-disrupting chemicals, such as polybrominated biphenyl (PBB), during fetal development and early life has been suspected to impact neurological development. This study aims to investigate the association between prenatal and early life exposure to PBB and the development of ADHD and autism later in life.\u0000 \u0000 \u0000 \u0000 Data from the Michigan PBB Registry, a cohort of Michigan residents who had been exposed to PBB in a mass contamination event in 1973, was leveraged for this nested case-control analysis among two distinct samples: (1) Those who self-reported ADHD or autism diagnosis, and (2) mothers who reported their child’s ADHD or autism diagnosis. PBB exposure was measured in participants of the PBB Registry, and the mother’s PBB level was used in mother-reported analyses. Cases were matched with controls by sex and year of birth. Conditional logistic regression models were used to estimate the association between PBB level and case status.\u0000 \u0000 \u0000 \u0000 PBB levels were higher among those who were exposed in early life compared with those exposed in utero (geometric mean: 0.300 ng/ml vs. 0.016 ng/ml). Among women in this cohort, a higher than expected proportion of self-reported ADHD diagnosis (11.11%), compared with population estimates. PBB was not associated with ADHD or autism in either self-reported or mother-reported analyses.\u0000 \u0000 \u0000 \u0000 This study adds to the sparse literature about prenatal and early life exposure to PBB-153 and ADHD and autism. Future studies should examine potential effect modification by sex.\u0000","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140247161","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 : 2024-03-12DOI: 10.1097/ee9.0000000000000299
Ruth A. Etzel, N. Abbas, Michael P. Anastario, A. Mustapha, Olayinka Osuolale, Atanu Sarkar, Ireneous N. Soyiri, Emile Whaibeh, Colin L. Soskolne
Recognition of the importance to environmental epidemiology of ethical and philosophical deliberation led, in 1996, to the establishment of Ethics Guidelines for the profession. In 1999, these guidelines were adopted by the International Society for Environmental Epidemiology. The guidelines were revised in 2012 and again in 2023 to ensure continued relevance to the major issues facing the field. Comprising normative standards of professional conduct, the guidelines are structured into four subsections: (1) obligations to individuals and communities who participate in research; (2) obligations to society; (3) obligations regarding funders/sponsors and employers; and (4) obligations to colleagues. Through the 2023 revision of the Ethics Guidelines, the International Society for Environmental Epidemiology seeks to ensure the highest possible standards of transparency and accountability for the ethical conduct of environmental epidemiologists engaged in research and public health practice.
{"title":"Ethics guidelines for environmental epidemiologists: 2023 revision","authors":"Ruth A. Etzel, N. Abbas, Michael P. Anastario, A. Mustapha, Olayinka Osuolale, Atanu Sarkar, Ireneous N. Soyiri, Emile Whaibeh, Colin L. Soskolne","doi":"10.1097/ee9.0000000000000299","DOIUrl":"https://doi.org/10.1097/ee9.0000000000000299","url":null,"abstract":"Recognition of the importance to environmental epidemiology of ethical and philosophical deliberation led, in 1996, to the establishment of Ethics Guidelines for the profession. In 1999, these guidelines were adopted by the International Society for Environmental Epidemiology. The guidelines were revised in 2012 and again in 2023 to ensure continued relevance to the major issues facing the field. Comprising normative standards of professional conduct, the guidelines are structured into four subsections: (1) obligations to individuals and communities who participate in research; (2) obligations to society; (3) obligations regarding funders/sponsors and employers; and (4) obligations to colleagues. Through the 2023 revision of the Ethics Guidelines, the International Society for Environmental Epidemiology seeks to ensure the highest possible standards of transparency and accountability for the ethical conduct of environmental epidemiologists engaged in research and public health practice.","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140249281","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 : 2024-03-11DOI: 10.1097/ee9.0000000000000302
Mahnaz Badpa, A. Schneider, Lars Schwettmann, Barbara Thorand, K. Wolf, A. Peters
Type 2 diabetes (T2D) is a major public health concern, and various environmental factors have been associated with the development of this disease. This study aimed to investigate the longitudinal effects of multiple environmental exposures on the risk of incident T2D in a German population-based cohort. We used data from the KORA cohort study (Augsburg, Germany) and assessed exposure to air pollutants, traffic noise, greenness, and temperature at the participants’ residencies. Cox proportional hazard models were used to analyze the associations with incident T2D, adjusting for potential confounders. Of 7736 participants included in the analyses, 10.5% developed T2D during follow-up (mean: 15.0 years). We found weak or no association between environmental factors and the risk of T2D, with sex and education level significantly modifying the effects of air pollutants. Our study contributes to the growing body of literature investigating the impact of environmental factors on T2D risks and suggests that the impact of environmental factors may be small.
{"title":"Air pollution, traffic noise, greenness, and temperature and the risk of incident type 2 diabetes: Results from the KORA cohort study","authors":"Mahnaz Badpa, A. Schneider, Lars Schwettmann, Barbara Thorand, K. Wolf, A. Peters","doi":"10.1097/ee9.0000000000000302","DOIUrl":"https://doi.org/10.1097/ee9.0000000000000302","url":null,"abstract":"\u0000 \u0000 Type 2 diabetes (T2D) is a major public health concern, and various environmental factors have been associated with the development of this disease. This study aimed to investigate the longitudinal effects of multiple environmental exposures on the risk of incident T2D in a German population-based cohort.\u0000 \u0000 \u0000 \u0000 We used data from the KORA cohort study (Augsburg, Germany) and assessed exposure to air pollutants, traffic noise, greenness, and temperature at the participants’ residencies. Cox proportional hazard models were used to analyze the associations with incident T2D, adjusting for potential confounders.\u0000 \u0000 \u0000 \u0000 Of 7736 participants included in the analyses, 10.5% developed T2D during follow-up (mean: 15.0 years). We found weak or no association between environmental factors and the risk of T2D, with sex and education level significantly modifying the effects of air pollutants.\u0000 \u0000 \u0000 \u0000 Our study contributes to the growing body of literature investigating the impact of environmental factors on T2D risks and suggests that the impact of environmental factors may be small.\u0000","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140252762","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 : 2024-03-07DOI: 10.1097/ee9.0000000000000301
T. VoPham, M. Ton, Matthew D. Weaver
Light exposure is the most powerful resetting signal for circadian rhythms. The objective of this study was to develop and validate a high-resolution geospatial light exposure model that measures environmental circadian misalignment (or solar jetlag) as the mismatch between the social clock and sun clock, which occurs from geographic variation in light exposure leading to delayed circadian phase from relatively less morning light exposure and greater evening light exposure with increasing westward position within a time zone. The light exposure model (30 m2 spatial resolution) incorporated geospatial data across the United States on time zones, elevation (using Google Earth Engine), sunrise time, and sunset time to estimate solar jetlag scores (higher values indicate higher environmental circadian misalignment). The validation study compared the light exposure model in 2022, which was linked with geocoded residential addresses of n = 20 participants in Boston, MA (eastern time zone position) and Seattle, WA (western time zone position) using a geographic information system, with illuminance values captured from wearable LYS light sensors and with sun times from the Solar Calculator. Western versus eastern positions within a time zone were associated with higher solar jetlag scores from the light exposure model (P < 0.01) and relatively larger differences in sunset time measured using light sensors (social clock) and the Solar Calculator (sun clock) (P = 0.04). We developed and validated a geospatial light exposure model, enabling high spatiotemporal resolution and comprehensive characterization of geographic variation in light exposure potentially impacting circadian phase in epidemiologic studies.
{"title":"Spatiotemporal light exposure modeling for environmental circadian misalignment and solar jetlag","authors":"T. VoPham, M. Ton, Matthew D. Weaver","doi":"10.1097/ee9.0000000000000301","DOIUrl":"https://doi.org/10.1097/ee9.0000000000000301","url":null,"abstract":"\u0000 \u0000 Light exposure is the most powerful resetting signal for circadian rhythms. The objective of this study was to develop and validate a high-resolution geospatial light exposure model that measures environmental circadian misalignment (or solar jetlag) as the mismatch between the social clock and sun clock, which occurs from geographic variation in light exposure leading to delayed circadian phase from relatively less morning light exposure and greater evening light exposure with increasing westward position within a time zone.\u0000 \u0000 \u0000 \u0000 The light exposure model (30 m2 spatial resolution) incorporated geospatial data across the United States on time zones, elevation (using Google Earth Engine), sunrise time, and sunset time to estimate solar jetlag scores (higher values indicate higher environmental circadian misalignment). The validation study compared the light exposure model in 2022, which was linked with geocoded residential addresses of n = 20 participants in Boston, MA (eastern time zone position) and Seattle, WA (western time zone position) using a geographic information system, with illuminance values captured from wearable LYS light sensors and with sun times from the Solar Calculator.\u0000 \u0000 \u0000 \u0000 Western versus eastern positions within a time zone were associated with higher solar jetlag scores from the light exposure model (P < 0.01) and relatively larger differences in sunset time measured using light sensors (social clock) and the Solar Calculator (sun clock) (P = 0.04).\u0000 \u0000 \u0000 \u0000 We developed and validated a geospatial light exposure model, enabling high spatiotemporal resolution and comprehensive characterization of geographic variation in light exposure potentially impacting circadian phase in epidemiologic studies.\u0000","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140259740","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 : 2024-03-07DOI: 10.1097/ee9.0000000000000297
Felipe Parra do Nascimento, Nelson Gouveia
There is a vast body of literature covering the association between air pollution exposure and nonaccidental mortality. However, the role of socioeconomic status (SES) in this relationship is still not fully understood. We investigated if individual and contextual SES modified the relationship between short-term exposure to ozone (O3), nitrogen dioxide (NO2), and particulate matter with aerodynamic diameter <10 µm (PM10) on cardiovascular, respiratory, and all nonaccidental mortality. We conducted a time-stratified case-crossover study. Analyses were based on information on 280,685 deaths from 2011 to 2015 in the city of São Paulo. Education was used as an individual SES, and information on the district of residence was used to build a contextual SES. Exposure to PM10, NO2, and O3 was accessed from monitoring stations and linked to each case based on the date of death. Conditional logistic regression models were used to estimate the effects of air pollutants, and interaction terms were added to access the effect modification of SES. Individuals with lower education had an increased chance of dying for all nonaccidental outcomes (1.54% [0.91%, 2.14%]) associated with exposure to PM10. Individuals living in lower SES areas had an increased chance of dying for nonaccidental (0.52% [0.16%, 0.88%]), cardiovascular (1.17% [0.88%, 1.46%]), and respiratory (1.70% [0.47%, 2.93%]) causes owing to NO2 exposure. Exposure to air pollutants increases the chance of dying by nonaccidental, cardiovascular, and respiratory causes. Lower educational levels and living on lower contextual SES increased the risk of mortality associated with air pollution exposure.
{"title":"Ambient air pollution and mortality: The role of socioeconomic conditions","authors":"Felipe Parra do Nascimento, Nelson Gouveia","doi":"10.1097/ee9.0000000000000297","DOIUrl":"https://doi.org/10.1097/ee9.0000000000000297","url":null,"abstract":"\u0000 \u0000 There is a vast body of literature covering the association between air pollution exposure and nonaccidental mortality. However, the role of socioeconomic status (SES) in this relationship is still not fully understood.\u0000 \u0000 \u0000 \u0000 We investigated if individual and contextual SES modified the relationship between short-term exposure to ozone (O3), nitrogen dioxide (NO2), and particulate matter with aerodynamic diameter <10 µm (PM10) on cardiovascular, respiratory, and all nonaccidental mortality.\u0000 \u0000 \u0000 \u0000 We conducted a time-stratified case-crossover study. Analyses were based on information on 280,685 deaths from 2011 to 2015 in the city of São Paulo. Education was used as an individual SES, and information on the district of residence was used to build a contextual SES. Exposure to PM10, NO2, and O3 was accessed from monitoring stations and linked to each case based on the date of death. Conditional logistic regression models were used to estimate the effects of air pollutants, and interaction terms were added to access the effect modification of SES.\u0000 \u0000 \u0000 \u0000 Individuals with lower education had an increased chance of dying for all nonaccidental outcomes (1.54% [0.91%, 2.14%]) associated with exposure to PM10. Individuals living in lower SES areas had an increased chance of dying for nonaccidental (0.52% [0.16%, 0.88%]), cardiovascular (1.17% [0.88%, 1.46%]), and respiratory (1.70% [0.47%, 2.93%]) causes owing to NO2 exposure.\u0000 \u0000 \u0000 \u0000 Exposure to air pollutants increases the chance of dying by nonaccidental, cardiovascular, and respiratory causes. Lower educational levels and living on lower contextual SES increased the risk of mortality associated with air pollution exposure.\u0000","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140077544","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 : 2024-02-29DOI: 10.1097/ee9.0000000000000296
Brooke L. Lappe, N. Scovronick, R. D'souza, Arie Manangan, Howard H. Chang, S. Ebelt
Pollen exposure is associated with substantial respiratory morbidity, but its potential impact on cardiovascular disease (CVD) remains less understood. This study aimed to investigate the associations between daily levels of 13 pollen types and emergency department (ED) visits for eight CVD outcomes over a 26-year period in Atlanta, GA. We acquired pollen data from Atlanta Allergy & Asthma, a nationally certified pollen counting station, and ED visit data from individual hospitals and the Georgia Hospital Association. We performed time-series analyses using quasi-Poisson distributed lag models, with primary analyses assessing 3-day (lag 0–2 days) pollen levels. Models controlled for temporally varying covariates, including air pollutants. During 1993–2018, there were 1,573,968 CVD ED visits. Most pairwise models of the 13 pollen types and eight CVD outcomes showed no association, with a few exceptions potentially due to chance. We found limited evidence of the impact of pollen on cardiovascular morbidity in Atlanta. Further study on pollen exposures in different climactic zones and exploration of pollen-pollution mixture effects is warranted.
{"title":"Associations of pollen and cardiovascular disease morbidity in Atlanta during 1993–2018","authors":"Brooke L. Lappe, N. Scovronick, R. D'souza, Arie Manangan, Howard H. Chang, S. Ebelt","doi":"10.1097/ee9.0000000000000296","DOIUrl":"https://doi.org/10.1097/ee9.0000000000000296","url":null,"abstract":"\u0000 \u0000 Pollen exposure is associated with substantial respiratory morbidity, but its potential impact on cardiovascular disease (CVD) remains less understood. This study aimed to investigate the associations between daily levels of 13 pollen types and emergency department (ED) visits for eight CVD outcomes over a 26-year period in Atlanta, GA.\u0000 \u0000 \u0000 \u0000 We acquired pollen data from Atlanta Allergy & Asthma, a nationally certified pollen counting station, and ED visit data from individual hospitals and the Georgia Hospital Association. We performed time-series analyses using quasi-Poisson distributed lag models, with primary analyses assessing 3-day (lag 0–2 days) pollen levels. Models controlled for temporally varying covariates, including air pollutants.\u0000 \u0000 \u0000 \u0000 During 1993–2018, there were 1,573,968 CVD ED visits. Most pairwise models of the 13 pollen types and eight CVD outcomes showed no association, with a few exceptions potentially due to chance.\u0000 \u0000 \u0000 \u0000 We found limited evidence of the impact of pollen on cardiovascular morbidity in Atlanta. Further study on pollen exposures in different climactic zones and exploration of pollen-pollution mixture effects is warranted.\u0000","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-02-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140409298","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 : 2024-02-19DOI: 10.1097/ee9.0000000000000292
Lisa Yamasaki, Takuma Kamada, C. Ng, Y. Takane, Ko Nakajima, Kazuki Yamaguchi, Kazutaka Oka, Yasushi Honda, Yoonhee Kim, Masahiro Hashizume
Air conditioners can prevent heat-related illness and mortality, but the increased use of air conditioners may enhance susceptibility to heat-related illnesses during large-scale power failures. Here, we examined the risks of heat-related illness ambulance transport (HIAT) and mortality associated with typhoon-related electricity reduction (ER) in the summer months in the Tokyo metropolitan area. We conducted event study analyses to compare temperature–HIAT and mortality associations before and after the power outage (July to September 2019). To better understand the role of temperature during the power outage, we then examined whether the temperature–HIAT and mortality associations were modified by different power outage levels (0%, 10%, and 20% ER). We computed the ratios of relative risks to compare the risks associated with various ER values to the risks associated without ER. We analyzed the data of 14,912 HIAT cases and 74,064 deaths. Overall, 93,200 power outage cases were observed when the typhoon hit. Event study results showed that the incidence rate ratio was 2.01 (95% confidence interval [CI] = 1.42, 2.84) with effects enduring up to 6 days, and 1.11 (95% CI = 1.02, 1.22) for mortality on the first 3 days after the typhoon hit. Comparing 20% to 0% ER, the ratios of relative risks of heat exposure were 2.32 (95% CI = 1.41, 3.82) for HIAT and 0.95 (95% CI = 0.75, 1.22) for mortality. A 20% ER was associated with a two-fold greater risk of HIAT because of summer heat during the power outage, but there was little evidence for the association with all-cause mortality.
{"title":"Heat-related mortality and ambulance transport after a power outage in the Tokyo metropolitan area","authors":"Lisa Yamasaki, Takuma Kamada, C. Ng, Y. Takane, Ko Nakajima, Kazuki Yamaguchi, Kazutaka Oka, Yasushi Honda, Yoonhee Kim, Masahiro Hashizume","doi":"10.1097/ee9.0000000000000292","DOIUrl":"https://doi.org/10.1097/ee9.0000000000000292","url":null,"abstract":"\u0000 \u0000 Air conditioners can prevent heat-related illness and mortality, but the increased use of air conditioners may enhance susceptibility to heat-related illnesses during large-scale power failures. Here, we examined the risks of heat-related illness ambulance transport (HIAT) and mortality associated with typhoon-related electricity reduction (ER) in the summer months in the Tokyo metropolitan area.\u0000 \u0000 \u0000 \u0000 We conducted event study analyses to compare temperature–HIAT and mortality associations before and after the power outage (July to September 2019). To better understand the role of temperature during the power outage, we then examined whether the temperature–HIAT and mortality associations were modified by different power outage levels (0%, 10%, and 20% ER). We computed the ratios of relative risks to compare the risks associated with various ER values to the risks associated without ER.\u0000 \u0000 \u0000 \u0000 We analyzed the data of 14,912 HIAT cases and 74,064 deaths. Overall, 93,200 power outage cases were observed when the typhoon hit. Event study results showed that the incidence rate ratio was 2.01 (95% confidence interval [CI] = 1.42, 2.84) with effects enduring up to 6 days, and 1.11 (95% CI = 1.02, 1.22) for mortality on the first 3 days after the typhoon hit. Comparing 20% to 0% ER, the ratios of relative risks of heat exposure were 2.32 (95% CI = 1.41, 3.82) for HIAT and 0.95 (95% CI = 0.75, 1.22) for mortality.\u0000 \u0000 \u0000 \u0000 A 20% ER was associated with a two-fold greater risk of HIAT because of summer heat during the power outage, but there was little evidence for the association with all-cause mortality.\u0000","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140451067","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}
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