Environmental Epidemiology最新文献

{"title":"Hurricane Harvey and the risk of spontaneous preterm and early-term birth","authors":"Xinyue Liu, Alique G. Berberian, Sophia Wang, Lara J. Cushing","doi":"10.1097/EE9.0000000000000312","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000312","url":null,"abstract":"Background: Hurricane Harvey made landfall in August 2017 and resulted in catastrophic flooding in Houston, Texas. Prior studies of hurricanes and preterm birth have found conflicting results. We tested the hypotheses that exposure to Hurricane Harvey was associated with a higher risk of spontaneous pre- and early-term birth and assessed vulnerable subpopulations. Methods: We conducted a retrospective study of singleton births using administrative birth records in the nine-county greater Houston area from 2015 to 2019. We estimated the likelihood of pre- and early-term births using logistic regression, comparing births occurring during or within 1, 2, or 4 weeks of Hurricane Harvey to unexposed reference periods encompassing the same dates 2 years prior and after. Stratified models assessed effect modification by degree of flooding, birth parent age, high- vs. low-risk pregnancy, race/ethnicity, and prenatal care. Results: Among 15,564 births, we found no association between exposure to Hurricane Harvey and spontaneous preterm birth within 1 week adjusted (odds ratio [OR], 1.06; 95% confidence interval [CI] = 0.91, 1.25) but a 14% higher odds of spontaneous early-term birth (OR, 1.14; 95% CI = 1.04, 1.25). The odds of early-term birth were even higher in neighborhoods with severe flooding (OR, 1.21; 95% CI = 1.05, 1.38), segregated neighborhoods (OR, 1.23; 95% CI = 1.03, 1.47), and among foreign-born Hispanics (OR, 1.21; 95% CI = 1.04, 1.53) and pregnant people receiving no prenatal care (OR, 1.37; 95% CI = 1.03, 1.82). Effect estimates were attenuated or null when considering 2-week or 4-week lags to define exposure. Conclusions: Hurricane Harvey was associated with higher odds of spontaneous early-term birth up to 1 week later, especially among socially marginalized populations.","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141126532","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fine particulate matter air pollution and health implications for Nairobi, Kenya","authors":"Otienoh Oguge, Joshua Nyamondo, Noah Adera, Lydia Okolla, Beldine Okoth, Stephen Anyango, Augustine Afulo, A. Kumie, Jonathan Samet, Kiros Berhane","doi":"10.1097/ee9.0000000000000307","DOIUrl":"https://doi.org/10.1097/ee9.0000000000000307","url":null,"abstract":"\u0000 \u0000 Continuous ambient air quality monitoring in Kenya has been limited, resulting in a sparse data base on the health impacts of air pollution for the country. We have operated a centrally located monitor in Nairobi for measuring fine particulate matter (PM2.5), the pollutant that has demonstrated impact on health. Here, we describe the temporal levels and trends in PM2.5 data for Nairobi and evaluate associated health implications.\u0000 \u0000 \u0000 \u0000 We used a centrally located reference sensor, the beta attenuation monitor (BAM-1022), to measure hourly PM2.5 concentrations over a 3-year period (21 August 2019 to 20 August 2022). We used, at minimum, 75% of the daily hourly concentration to represent the 24-hour concentrations for a given calendar day. To estimate the deaths attributable to air pollution, we used the World Health Organization (WHO) AirQ+ tool with input as PM2.5 concentration data, local mortality statistics, and population sizes.\u0000 \u0000 \u0000 \u0000 The daily (24-hour) mean (±SEM) PM2.5 concentration was 19. 2 ± 0.6 (µg/m3). Pollutant levels were lowest at 03:00 and, peaked at 20:00. Sundays had the lowest daily concentrations, which increased on Mondays and remained high through Saturdays. By season, the pollutant concentrations were lowest in April and highest in August. The mean annual concentration was 18.4 ± 7.1 (µg/m3), which was estimated to lead to between 400 and 1,400 premature deaths of the city’s population in 2021 hence contributing 5%–8% of the 17,432 adult deaths excluding accidents when referenced to WHO recommended 2021 air quality guideline for annual thresholds of 5 µg/m3.\u0000 \u0000 \u0000 \u0000 Fine particulate matter air pollution in Nairobi showed daily, day-of-week, and seasonal fluctuations consistent with the anthropogenic source mix, particularly from motor vehicles. The long-term population exposure to PM2.5 was 3.7 times higher than the WHO annual guideline of 5 µg/m3 and estimated to lead to a substantial burden of attributable deaths. An updated regulation targeting measures to reduce vehicular emissions is recommended.\u0000","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140694622","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An assessment of the mediating role of hypertension in the effect of long-term air pollution exposure on dementia","authors":"Tanya E. Libby, S. Ilango, C. Leary, E. Semmens, Claire E Adam, Annette L. Fitzpatrick, J. Kaufman, A. Hajat","doi":"10.1097/ee9.0000000000000306","DOIUrl":"https://doi.org/10.1097/ee9.0000000000000306","url":null,"abstract":"\u0000 \u0000 Growing evidence links air pollution exposure to the risk of dementia. We hypothesized that hypertension may partially mediate this effect.\u0000 \u0000 \u0000 \u0000 We previously documented an association between air pollution and dementia in the Ginkgo Evaluation of Memory Study, a randomized, placebo-controlled trial of 3069 adults ≥75 years across four US sites who were evaluated for dementia every 6 months from 2000–2008. We utilized a two-stage regression approach for causal mediation analysis to decompose the total effect of air pollution on dementia into its natural direct and indirect effect through prevalent hypertension. Exposure to air pollution in the 10 or 20 years before enrollment was assigned using estimates from fine-scale spatial-temporal models for PM2.5, PM10, and NO2. We used Poisson regression models for hypertension and Cox proportional hazard models for time-to-incident all-cause dementia, adjusting for a priori confounders.\u0000 \u0000 \u0000 \u0000 Participants were free of mild cognitive impairment at baseline (n = 2564 included in analyses); 69% had prevalent hypertension at baseline. During follow-up, 12% developed all-cause dementia (Alzheimer’s disease [AD] = 212; vascular dementia with or without AD [VaD/AD mixed] = 97). We did not find an adverse effect of any air pollutant on hypertension. Hypertension was associated with VaD/AD mixed (HR, 1.92 [95% CI = 1.14, 3.24]) but not AD. We did not observe mediation through hypertension for the effect of any pollutant on dementia outcomes.\u0000 \u0000 \u0000 \u0000 The lack of mediated effect may be due to other mechanistic pathways and the minimal effect of air pollution on hypertension in this cohort of older adults.\u0000","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140711235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Increased vascular stiffness in children exposed in utero but not children exposed postnatally to emissions from a coal mine fire","authors":"Emily J. Hemstock, Ashley Bigaran, S. Allgood, Amanda J. Wheeler, M. Dalton, Grant J. Williamson, Caroline X. Gao, Michael J. Abramson, Kazuaki Negishi, F. Johnston, G. Zosky","doi":"10.1097/ee9.0000000000000309","DOIUrl":"https://doi.org/10.1097/ee9.0000000000000309","url":null,"abstract":"\u0000 \u0000 Chronic, low-intensity air pollution exposure has been consistently associated with increased atherosclerosis in adults. However, there was limited research regarding the implications of acute, high-intensity air pollution exposure during childhood. We aimed to determine whether there were any associations between early-life exposure to such an episode and early-life vascular function changes.\u0000 \u0000 \u0000 \u0000 We conducted a prospective cohort study of children (<9 years old) who lived in the vicinity of the Hazelwood coal mine fire (n = 206). Vascular function was measured using noninvasive diagnostic methods including carotid intima-media thickness and pulse wave velocity (PWV). Exposure estimates were calculated from prognostic models and location diaries during the exposure period completed by each participant’s parent. Linear mixed-effects models were used to determine whether there were any associations between exposure and changes in vascular outcomes at the 3- and 7-year follow-ups and over time.\u0000 \u0000 \u0000 \u0000 At the 7-year follow-up, each 10 μg/m3 increase in daily PM2.5 in utero was associated with increased PWV (β = 0.13 m/s; 95% confidence interval [CI] = 0.02, 0.24; P = 0.02). The association between in utero exposure to daily PM2.5 was not altered by adjustment for covariates, body mass index, and maternal fire stress. Each 1 µg/m3 increase in background PM2.5 was associated with increased PWV (β = 0.68 m/s; 95% CI = 0.10, 1.26; P = 0.025), in children from the in utero exposure group. There was a trend toward smaller PWV (β = −0.17 m/s; 95% CI = −0.366, 0.02) from the 3- to 7-year follow-up clinic suggesting that the deficits observed previously in children exposed postnatally did not persist.\u0000 \u0000 \u0000 \u0000 There was a moderate improvement in vascular stiffness of children exposed to PM2.5 from a local coal mine fire in infancy. There was a mild increase in vascular stiffness in children exposed to PM2.5 from a local coal mine fire while their mothers were pregnant.\u0000","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140710507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Longitudinal associations between ambient PM_2.5 exposure and lipid levels in two Indian cities.","authors":"Kritika Anand, Gagandeep Kaur Walia, Siddhartha Mandal, Jyothi S Menon, Ruby Gupta, Nikhil Tandon, K M Venkat Narayan, Mohammed K Ali, Viswanathan Mohan, Joel D Schwartz, Dorairaj Prabhakaran","doi":"10.1097/EE9.0000000000000295","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000295","url":null,"abstract":"<p><strong>Background: </strong>Exposure to ambient PM_2.5 is known to affect lipid metabolism through systemic inflammation and oxidative stress. Evidence from developing countries, such as India with high levels of ambient PM_2.5 and distinct lipid profiles, is sparse.</p><p><strong>Methods: </strong>Longitudinal nonlinear mixed-effects analysis was conducted on >10,000 participants of Centre for cArdiometabolic Risk Reduction in South Asia (CARRS) cohort in Chennai and Delhi, India. We examined associations between 1-month and 1-year average ambient PM_2.5 exposure derived from the spatiotemporal model and lipid levels (total cholesterol [TC], triglycerides [TRIG], high-density lipoprotein cholesterol [HDL-C], and low-density lipoprotein cholesterol [LDL-C]) measured longitudinally, adjusting for residential and neighborhood-level confounders.</p><p><strong>Results: </strong>The mean annual exposure in Chennai and Delhi was 40 and 102 μg/m³ respectively. Elevated ambient PM_2.5 levels were associated with an increase in LDL-C and TC at levels up to 100 µg/m³ in both cities and beyond 125 µg/m³ in Delhi. TRIG levels in Chennai increased until 40 µg/m³ for both short- and long-term exposures, then stabilized or declined, while in Delhi, there was a consistent rise with increasing annual exposures. HDL-C showed an increase in both cities against monthly average exposure. HDL-C decreased slightly in Chennai with an increase in long-term exposure, whereas it decreased beyond 130 µg/m³ in Delhi.</p><p><strong>Conclusion: </strong>These findings demonstrate diverse associations between a wide range of ambient PM_2.5 and lipid levels in an understudied South Asian population. Further research is needed to establish causality and develop targeted interventions to mitigate the impact of air pollution on lipid metabolism and cardiovascular health.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11008625/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140850045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"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}

{"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}

{"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}

{"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}

{"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}