Environmental Epidemiology最新文献

{"title":"The destruction of Gaza's infrastructure is exacerbating environmental health impacts.","authors":"Adnan Al-Hindi, Amira Aker, Wael K Al-Delaimy","doi":"10.1097/EE9.0000000000000186","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000186","url":null,"abstract":"","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":" ","pages":"e186"},"PeriodicalIF":3.6,"publicationDate":"2021-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/1d/9b/ee9-6-e186.PMC8835639.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39624142","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":"The influence of outdoor PM_2.5 concentration at workplace on nonaccidental mortality estimates in a Canadian census-based cohort.","authors":"Tanya Christidis,&nbsp;Lauren L Pinault,&nbsp;Dan L Crouse,&nbsp;Michael Tjepkema","doi":"10.1097/EE9.0000000000000180","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000180","url":null,"abstract":"<p><strong>Background: </strong>Associations between mortality and exposure to ambient air pollution are usually explored using concentrations of residential outdoor fine particulate matter (PM_2.5) to estimate individual exposure. Such studies all have an important limitation in that they do not capture data on individual mobility throughout the day to areas where concentrations may be substantially different, leading to possible exposure misclassification. We examine the possible role of outdoor PM_2.5 concentrations at work for a large population-based mortality cohort.</p><p><strong>Methods: </strong>Using the 2001 Canadian Census Health and Environment Cohort (CanCHEC), we created a time-weighted average that incorporates employment hours worked in the past week and outdoor PM_2.5 concentration at work and home. We used a Cox proportional hazard model with a 15-year follow-up (2001 to 2016) to explore whether inclusion of workplace estimates had an impact on hazard ratios for mortality for this cohort.</p><p><strong>Results: </strong>Hazard ratios relying on outdoor PM_2.5 concentration at home were not significantly different from those using a time-weighted estimate, for the full cohort, nor for those who commute to a regular workplace. When exploring cohort subgroups according to neighborhood type and commute distance, there was a notable but insignificant change in risk of nonaccidental death for those living in car-oriented neighborhoods, and with commutes greater than 10 km.</p><p><strong>Conclusions: </strong>Risk analyses performed with large cohorts in low-pollution environments do not seem to be biased if relying solely on outdoor PM_2.5 concentrations at home to estimate exposure.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":" ","pages":"e180"},"PeriodicalIF":3.6,"publicationDate":"2021-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/13/86/ee9-5-e180.PMC8663884.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39589214","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":"Epidemiology and biological plausibility in assessing causality.","authors":"David A Savitz","doi":"10.1097/EE9.0000000000000177","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000177","url":null,"abstract":"One of the well-accepted principles of epidemiology is the need to draw upon ancillary evidence from biological research in the selection of topics to pursue, design of studies, and especially, the interpretation of the results. In environmental epidemiology, understanding the biological pathways by which the exposure of concern may affect health often has a great value in framing research questions and guiding the studies that are done but calls for deeper reflection of how that ancillary biological information should (and should not) be used. Biological evidence of potential health harm may motivate epidemiologic studies and help to guide exposure assessment to maximize the likelihood of identifying an etiologic relationship if one is present. Decisions regarding exposure aggregation (lumping or splitting), duration of exposure, the timing of exposure in relation to disease occurrence, exploration of dose-response patterns (thresholds and ceilings), and other chemical and physical features of exposure to be examined in epidemiologic studies benefit from drawing on knowledge from pertinent biological research. Similarly, the choice of specific disease entities should be informed by knowledge of biological mechanisms in the analogous decisions regarding grouping, timing of onset, distinctive features of the disease (e.g., subsets of cancer with a shared etiology), and clinical manifestations. Markers of susceptibility that could result in effect-modification may be gleaned from biological research as well as candidate confounders. The product of this knowledge drawn from work done in other fields, if considered in advance, is an enhanced ability to design and conduct epidemiologic studies in which the measure of association is most likely to identify any causal effects that are present, that is, more valid studies. If positive or negative associations are found, they would be seen as concordant with expectations based on biology and if null associations are found, this would provide meaningful evidence that the plausible etiologic relationship is not likely to be present. But the dividing line between using biological evidence to optimize the design of studies and the use of biological evidence to render a verdict on the validity of the study calls for a closer look. The consideration of biological plausibility in the interpretation of the study results, as advocated by Sir Austin Bradford Hill1 raises some concerns when considering why measured associations may or may not reflect a causal effect. To the extent that the epidemiologic research is informed by sound biological insights, we will benefit from having focused on the most pertinent exposure and disease measures, minimizing exposure and disease misclassification, and isolating the most highly susceptible subgroups. Once we have gleaned all that we can from ancillary biological research on the topic, however, the epidemiologic study must stand on its merits in order to approximate the caus","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":" ","pages":"e177"},"PeriodicalIF":3.6,"publicationDate":"2021-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8663842/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39589211","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ambient temperature and stillbirth risks in northern Sweden, 1880-1950.","authors":"Lena Karlsson,&nbsp;Johan Junkka,&nbsp;Erling Häggström Lundevaller,&nbsp;Barbara Schumann","doi":"10.1097/EE9.0000000000000176","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000176","url":null,"abstract":"<p><strong>Background: </strong>Climate vulnerability of the unborn can contribute to adverse birth outcomes, in particular, but it is still not well understood. We investigated the association between ambient temperature and stillbirth risk among a historical population in northern Sweden (1880-1950).</p><p><strong>Methods: </strong>We used digitized parish records and daily temperature data from the study region covering coastal and inland communities some 600 km north of Stockholm, Sweden. The data included 141,880 births, and 3,217 stillbirths, corresponding to a stillbirth rate of 22.7 (1880-1950). The association between lagged temperature (0-7 days before birth) and stillbirths was estimated using a time-stratified case-crossover design. Incidence risk ratios (IRR) with 95% confidence intervals were computed, and stratified by season and sex.</p><p><strong>Results: </strong>We observed that the stillbirth risk increased both at low and high temperatures during the extended summer season (April to September), at -10°C, and the IRR was 2.3 (CI 1.28, 4.00) compared to the minimum mortality temperature of +15°C. No clear effect of temperature during the extended winter season (October to March) was found. Climate vulnerability was greater among the male fetus compared to the female counterparts.</p><p><strong>Conclusion: </strong>In this subarctic setting before and during industrialization, both heat and cold during the warmer season increased the stillbirth risk. Urbanization and socio-economic development might have contributed to an uneven decline in climate vulnerability of the unborn.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":" ","pages":"e176"},"PeriodicalIF":3.6,"publicationDate":"2021-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/27/10/ee9-5-e176.PMC8663868.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39589210","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ambient air pollution associated with lower academic achievement among US children: A nationwide panel study of school districts.","authors":"Wenxin Lu,&nbsp;Daniel A Hackman,&nbsp;Joel Schwartz","doi":"10.1097/EE9.0000000000000174","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000174","url":null,"abstract":"<p><strong>Background: </strong>Ambient air pollution is an important environmental exposure and has been linked with impaired cognitive function. Few studies have investigated its impact on children's academic performance on a nationwide level. We hypothesize that higher ambient air pollution concentrations will be associated with lower average academic test scores.</p><p><strong>Methods: </strong>We investigated three prevalent ambient air pollutants: PM_2.5, NO₂ and ozone, and their associations with the average academic test scores, at the Geographic School District (GSD) level, of the third to eighth grade students in the United States from 2010 to 2016. We applied multivariate linear regression and controlled for urbanicity, socioeconomic status, student racial/ethnic compositions, and individual intercepts for each district-grade level and each year.</p><p><strong>Results: </strong>We found that an interquartile range increase in PM_2.5 concentrations was associated with a 0.007 (95% confidence interval: 0.005, 0.009) SD lower average math test scores, and a 0.004 (95% confidence interval: 0.002, 0.005) SD lower average English language/arts test scores. Similar associations were observed for NO₂ and ozone on math, and for NO₂ on English language/arts. The magnitudes of these associations are equivalent to the effects of short-term reductions of thousands of dollars in district median household income. The reductions in test scores were larger for GSDs with higher socioeconomic status, though most associations remained negative at all socioeconomic levels.</p><p><strong>Conclusions: </strong>Our results show that ambient air pollution within a GSD is associated with lower academic performance among children. Further improving air quality may benefit children's overall academic achievement and socioeconomic attainment across the lifespan.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":" ","pages":"e174"},"PeriodicalIF":3.6,"publicationDate":"2021-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/56/8b/ee9-5-e174.PMC8663889.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39589209","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":"Residential proximity to hydraulically fractured oil and gas wells and adverse birth outcomes in urban and rural communities in California (2006-2015).","authors":"Kathy V Tran,&nbsp;Joan A Casey,&nbsp;Lara J Cushing,&nbsp;Rachel Morello-Frosch","doi":"10.1097/EE9.0000000000000172","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000172","url":null,"abstract":"<p><strong>Background: </strong>Prenatal exposure to hydraulic fracturing (HF), a chemically intensive oil and gas extraction method, may be associated with adverse birth outcomes, but no health studies have been conducted in California.</p><p><strong>Methods: </strong>We conducted a retrospective cohort study of 979,961 births to mothers in eight California counties with HF between 2006 and 2015. Exposed individuals had at least 1 well hydraulically fractured within 1 km of their residence during pregnancy; the reference population had no wells within 1 km, but at least one oil/gas well within 10 km. We examined associations between HF and low birth weight (LBW), preterm birth (PTB), small for gestational age birth (SGA), and term birth weight (tBW) using generalized estimating equations and assessing urban-rural effect modification in stratified models.</p><p><strong>Results: </strong>Fewer than 1% of mothers (N = 1,192) were exposed to HF during pregnancy. Among rural mothers, HF exposure was associated with increased odds of LBW (odds ratio [OR] = 1.74; 95% confidence interval [CI] = 1.10, 2.75), SGA (OR = 1.68; 95% CI = 1.42, 2.27) and PTB (OR = 1.17; 95% CI = 0.64, 2.12), and lower tBW (mean difference: -73 g; 95% CI = -131, -15). Among urban mothers, HF exposure was positively associated with SGA (OR = 1.23; 95% CI = 0.98, 1.55), inversely associated with LBW (OR = 0.83; 95% CI = 0.63, 1.07) and PTB (OR = 0.65; 95% CI = 0.48, 0.87), and not associated with tBW (mean difference: -2 g; 95% CI = -35, 31).</p><p><strong>Conclusion: </strong>HF proximity was associated with adverse birth outcomes, particularly among rural Californians.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":" ","pages":"e172"},"PeriodicalIF":3.6,"publicationDate":"2021-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/d2/d4/ee9-5-e172.PMC8663888.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39728310","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":"Geographical Variations of the Minimum Mortality Temperature at a Global Scale: A Multicountry Study.","authors":"Aurelio Tobías, Masahiro Hashizume, Yasushi Honda, Francesco Sera, Chris Fook Sheng Ng, Yoonhee Kim, Dominic Roye, Yeonseung Chung, Tran Ngoc Dang, Ho Kim, Whanhee Lee, Carmen Íñiguez, Ana Vicedo-Cabrera, Rosana Abrutzky, Yuming Guo, Shilu Tong, Micheline de Sousa Zanotti Stagliorio Coelho, Paulo Hilario Nascimento Saldiva, Eric Lavigne, Patricia Matus Correa, Nicolás Valdés Ortega, Haidong Kan, Samuel Osorio, Jan Kyselý, Aleš Urban, Hans Orru, Ene Indermitte, Jouni J K Jaakkola, Niilo R I Ryti, Mathilde Pascal, Veronika Huber, Alexandra Schneider, Klea Katsouyanni, Antonis Analitis, Alireza Entezari, Fatemeh Mayvaneh, Patrick Goodman, Ariana Zeka, Paola Michelozzi, Francesca de'Donato, Barrak Alahmad, Magali Hurtado Diaz, César De la Cruz Valencia, Ala Overcenco, Danny Houthuijs, Caroline Ameling, Shilpa Rao, Francesco Di Ruscio, Gabriel Carrasco, Xerxes Seposo, Baltazar Nunes, Joana Madureira, Iulian-Horia Holobaca, Noah Scovronick, Fiorella Acquaotta, Bertil Forsberg, Christofer Åström, Martina S Ragettli, Yue-Liang Leon Guo, Bing-Yu Chen, Shanshan Li, Valentina Colistro, Antonella Zanobetti, Joel Schwartz, Do Van Dung, Ben Armstrong, Antonio Gasparrini","doi":"10.1097/EE9.0000000000000169","DOIUrl":"10.1097/EE9.0000000000000169","url":null,"abstract":"<p><strong>Background: </strong>Minimum mortality temperature (MMT) is an important indicator to assess the temperature-mortality association, indicating long-term adaptation to local climate. Limited evidence about the geographical variability of the MMT is available at a global scale.</p><p><strong>Methods: </strong>We collected data from 658 communities in 43 countries under different climates. We estimated temperature-mortality associations to derive the MMT for each community using Poisson regression with distributed lag nonlinear models. We investigated the variation in MMT by climatic zone using a mixed-effects meta-analysis and explored the association with climatic and socioeconomic indicators.</p><p><strong>Results: </strong>The geographical distribution of MMTs varied considerably by country between 14.2 and 31.1 °C decreasing by latitude. For climatic zones, the MMTs increased from alpine (13.0 °C) to continental (19.3 °C), temperate (21.7 °C), arid (24.5 °C), and tropical (26.5 °C). The MMT percentiles (MMTPs) corresponding to the MMTs decreased from temperate (79.5th) to continental (75.4th), arid (68.0th), tropical (58.5th), and alpine (41.4th). The MMTs indreased by 0.8 °C for a 1 °C rise in a community's annual mean temperature, and by 1 °C for a 1 °C rise in its SD. While the MMTP decreased by 0.3 centile points for a 1 °C rise in a community's annual mean temperature and by 1.3 for a 1 °C rise in its SD.</p><p><strong>Conclusions: </strong>The geographical distribution of the MMTs and MMTPs is driven mainly by the mean annual temperature, which seems to be a valuable indicator of overall adaptation across populations. Our results suggest that populations have adapted to the average temperature, although there is still more room for adaptation.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":" ","pages":"e169"},"PeriodicalIF":3.3,"publicationDate":"2021-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/32/9b/ee9-5-e169.PMC8683148.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39745622","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ambient air pollution and inflammatory effects in a Canadian pregnancy cohort.","authors":"Priyanka Gogna,&nbsp;Will D King,&nbsp;Paul J Villeneuve,&nbsp;Premkumari Kumarathasan,&nbsp;Markey Johnson,&nbsp;Bruce Lanphear,&nbsp;Robin H Shutt,&nbsp;Tye E Arbuckle,&nbsp;Michael M Borghese","doi":"10.1097/EE9.0000000000000168","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000168","url":null,"abstract":"<p><strong>Background: </strong>Epidemiologic studies have consistently reported associations between air pollution and pregnancy outcomes including preeclampsia and gestational diabetes. However, the biologic mechanisms underlying these relationships remain unclear as few studies have collected relevant biomarker data. We examined relationships between ambient PM_2.5 and NO₂ with markers of inflammation during pregnancy in a prospective cohort of Canadian women.</p><p><strong>Methods: </strong>We analyzed data from 1170 women enrolled in the Maternal-Infant Research on Environmental Chemicals study. Daily residential PM_2.5 and NO₂ exposures during pregnancy were estimated using satellite-based and land-use regression models and used to create 14-day and 30-day exposure windows before blood-draw. Inflammatory markers C-reactive protein, interleukin-6, interleukin-8, and tumor necrosis factor-α were measured in third trimester plasma samples. Multivariable linear regression was used to estimate associations for an interquartile range (IQR) increase in PM_2.5 and NO₂ and markers of inflammation, while adjusting for individual-level confounders.</p><p><strong>Results: </strong>Fourteen-day (IQR: 6.85 µg/m³) and 30-day (IQR: 6.15 µg/m³) average PM_2.5 exposures before blood-draw were positively associated with C-reactive protein after adjustment for covariates (24.6% [95% CI = 9.4, 41.9] and 17.4% [95% CI = 1.0, 35.0] increases, respectively). This association was found to be robust in several sensitivity analyses. Neither PM_2.5 nor NO₂ exposures were associated with interleukin-6, interleukin-8, or tumor necrosis factor-α.</p><p><strong>Conclusion: </strong>Exposure to ambient PM_2.5 is positively associated with maternal inflammatory pathways in late pregnancy. This may contribute to positive associations between ambient PM_2.5 and risk of adverse pregnancy outcomes.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":" ","pages":"e168"},"PeriodicalIF":3.6,"publicationDate":"2021-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/f9/ce/ee9-5-e168.PMC8683146.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39834922","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":"Does early life phthalate exposure mediate racial disparities in children’s cognitive abilities?","authors":"M. Patti, M. Eliot, Nan Li, K. Yolton, B. Lanphear, Aimin Chen, J. Braun","doi":"10.1097/EE9.0000000000000205","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000205","url":null,"abstract":"Background: Early life exposure to phthalates may be associated with reduced cognition. However, it is unknown if disproportionate exposure to phthalates contributes to racial disparities in children’s intellectual abilities. Methods: We used data from 253 mother-child pairs in Cincinnati, OH (the Health Outcomes and Measures of the Environment study, 2003–2006). We measured urinary concentrations of 11 phthalate metabolites twice during pregnancy and up to six times in childhood. We evaluated children’s cognitive abilities at ages 5 and 8 years. Using mediation models, we quantified covariate-adjusted direct and indirect effects of race on children’s Full-Scale Intelligence Quotient (IQ) scores for individual phthalate metabolite concentrations during gestation and childhood. Results: Average IQ scores among Black children (n = 90) were 7.0 points lower (95% confidence interval [CI] = −12, −1.8) than among White children (n = 145) after adjustment for socioeconomic factors. Urinary monobenzyl phthalate and monoethyl phthalate (MEP) concentrations during gestation and childhood were higher among Black than White children. We did not observe evidence that phthalate concentrations mediated the race-IQ association, with the exception of MEP. Childhood MEP concentrations partially mediated the race-IQ association. For instance, each 10-fold increase in MEP concentrations at age 2 years contributed to a 1.9-point disparity in IQ scores between Black and White children (95% CI = −4.7, 0.7). Other phthalate metabolite concentrations during pregnancy or childhood did not mediate the race-IQ association. Conclusions: Despite observing racial disparities in exposure to some phthalates and IQ, we found little evidence that phthalates contribute to IQ disparities.","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":"6 1","pages":""},"PeriodicalIF":3.6,"publicationDate":"2021-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44695288","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":"Daily nonaccidental mortality associated with short-term PM_2.5 exposures in Delhi, India.","authors":"Bhargav Krishna,&nbsp;Siddhartha Mandal,&nbsp;Kishore Madhipatla,&nbsp;K Srinath Reddy,&nbsp;Dorairaj Prabhakaran,&nbsp;Joel D Schwartz","doi":"10.1097/EE9.0000000000000167","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000167","url":null,"abstract":"<p><p>Ambient particulate matter of aerodynamic diameter less than 2.5 microns PM_2.5) levels in Delhi routinely exceed World Health Organization (WHO) guidelines and Indian National Ambient Air Quality Standards (NAAQS) for acceptable levels of daily exposure. Only a handful of studies have examined the short-term mortality effects of PM in India, with none from Delhi examining the contribution of PM_2.5.</p><p><strong>Objectives: </strong>We aimed to analyze the association between short-term PM_2.5 exposures and daily nonaccidental mortality in Delhi, India.</p><p><strong>Methods: </strong>Using generalized additive Poisson regression models, we examined the association between daily PM_2.5 exposures and nonaccidental mortality between June 2010 and December 2016. Daily exposures to PM_2.5 were estimated using an ensemble averaging technique developed by our research group, and mortality data were obtained from the Municipal Corporations of Delhi and the New Delhi Municipal Council.</p><p><strong>Results: </strong>Median exposures to PM_2.5 were 91.1 µg/m³ (interquartile range = 68.9, 126.2), with minimum and maximum exposures of 21.4 µg/m³ and 276.7 µg/m³, respectively. Total nonaccidental deaths recorded in Delhi during the study period were 700,512. Each 25 µg/m³ increment in exposure was associated with a 0.8% (95% confidence intervals [CI] = 0.3, 1.3%) increase in daily nonaccidental mortality in the study population and a 1.5% (95% CI = 0.8, 2.2%) increase in mortality among those with 60 years of age or over. The exposure-response relationship was nonlinear in nature, with relative risk rising rapidly before tapering off above 125 µg/m³. Meeting WHO guidelines for acceptable levels of exposure over the study period would have likely averted 17,526 (95% CI = 6,837, 25,589) premature deaths, with older and male populations disproportionately affected.</p><p><strong>Discussion: </strong>This study provides robust evidence of the impact of short-term exposure to PM_2.5 on nonaccidental mortality with important considerations for various stakeholders including policymakers and physicians. Most importantly, we find that reducing exposures significantly below current levels would substantially decrease the mortality burden associated with PM_2.5.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":" ","pages":"e167"},"PeriodicalIF":3.6,"publicationDate":"2021-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/d7/47/ee9-5-e167.PMC8367036.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39330833","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}