Pub Date : 2024-05-07DOI: 10.1186/s12940-024-01077-z
Saira Tasmin, Briseis Aschebrook-Kilfoy, Donald Hedeker, Rajan Gopalakrishnan, Elizabeth Connellan, Muhammad G Kibriya, Michael T Young, Joel D Kaufman, Habibul Ahsan
Objectives: To examine whether long-term air pollution exposure is associated with central hemodynamic and brachial artery stiffness parameters.
Methods: We assessed central hemodynamic parameters including central blood pressure, cardiac parameters, systemic vascular compliance and resistance, and brachial artery stiffness measures [including brachial artery distensibility (BAD), compliance (BAC), and resistance (BAR)] using waveform analysis of the arterial pressure signals obtained from a standard cuff sphygmomanometer (DynaPulse2000A, San Diego, CA). The long-term exposures to particles with an aerodynamic diameter < 2.5 μm (PM2.5) and nitrogen dioxide (NO2) for the 3-year periods prior to enrollment were estimated at residential addresses using fine-scale intra-urban spatiotemporal models. Linear mixed models adjusted for potential confounders were used to examine associations between air pollution exposures and health outcomes.
Results: The cross-sectional study included 2,387 Chicago residents (76% African Americans) enrolled in the ChicagO Multiethnic Prevention And Surveillance Study (COMPASS) during 2013-2018 with validated address information, PM2.5 or NO2, key covariates, and hemodynamics measurements. We observed long-term concentrations of PM2.5 and NO2 to be positively associated with central systolic, pulse pressure and BAR, and negatively associated with BAD, and BAC after adjusting for relevant covariates. A 1-µg/m3 increment in preceding 3-year exposures to PM2.5 was associated with 1.8 mmHg higher central systolic (95% CI: 0.98, 4.16), 1.0 mmHg higher central pulse pressure (95% CI: 0.42, 2.87), a 0.56%mmHg lower BAD (95% CI: -0.81, -0.30), and a 0.009 mL/mmHg lower BAC (95% CI: -0.01, -0.01).
Conclusion: This population-based study provides evidence that long-term exposures to PM2.5 and NO2 is related to central BP and arterial stiffness parameters, especially among African Americans.
{"title":"Long-term exposure to ambient air pollution and measures of central hemodynamics and arterial stiffness among multiethnic Chicago residents.","authors":"Saira Tasmin, Briseis Aschebrook-Kilfoy, Donald Hedeker, Rajan Gopalakrishnan, Elizabeth Connellan, Muhammad G Kibriya, Michael T Young, Joel D Kaufman, Habibul Ahsan","doi":"10.1186/s12940-024-01077-z","DOIUrl":"10.1186/s12940-024-01077-z","url":null,"abstract":"<p><strong>Objectives: </strong>To examine whether long-term air pollution exposure is associated with central hemodynamic and brachial artery stiffness parameters.</p><p><strong>Methods: </strong>We assessed central hemodynamic parameters including central blood pressure, cardiac parameters, systemic vascular compliance and resistance, and brachial artery stiffness measures [including brachial artery distensibility (BAD), compliance (BAC), and resistance (BAR)] using waveform analysis of the arterial pressure signals obtained from a standard cuff sphygmomanometer (DynaPulse2000A, San Diego, CA). The long-term exposures to particles with an aerodynamic diameter < 2.5 μm (PM2.5) and nitrogen dioxide (NO2) for the 3-year periods prior to enrollment were estimated at residential addresses using fine-scale intra-urban spatiotemporal models. Linear mixed models adjusted for potential confounders were used to examine associations between air pollution exposures and health outcomes.</p><p><strong>Results: </strong>The cross-sectional study included 2,387 Chicago residents (76% African Americans) enrolled in the ChicagO Multiethnic Prevention And Surveillance Study (COMPASS) during 2013-2018 with validated address information, PM2.5 or NO2, key covariates, and hemodynamics measurements. We observed long-term concentrations of PM2.5 and NO2 to be positively associated with central systolic, pulse pressure and BAR, and negatively associated with BAD, and BAC after adjusting for relevant covariates. A 1-µg/m<sup>3</sup> increment in preceding 3-year exposures to PM2.5 was associated with 1.8 mmHg higher central systolic (95% CI: 0.98, 4.16), 1.0 mmHg higher central pulse pressure (95% CI: 0.42, 2.87), a 0.56%mmHg lower BAD (95% CI: -0.81, -0.30), and a 0.009 mL/mmHg lower BAC (95% CI: -0.01, -0.01).</p><p><strong>Conclusion: </strong>This population-based study provides evidence that long-term exposures to PM2.5 and NO2 is related to central BP and arterial stiffness parameters, especially among African Americans.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11075200/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140876105","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-04DOI: 10.1186/s12940-024-01084-0
Danielle Vienneau, Benedikt Wicki, Benjamin Flückiger, Beat Schäffer, Jean Marc Wunderli, Martin Röösli
Long-term exposure to transportation noise is related to cardio-metabolic diseases, with more recent evidence also showing associations with diabetes mellitus (DM) incidence. This study aimed to evaluate the association between transportation noise and DM mortality within the Swiss National Cohort. During 15 years of follow-up (2001–2015; 4.14 million adults), over 72,000 DM deaths were accrued. Source-specific noise was calculated at residential locations, considering moving history. Multi-exposure, time-varying Cox regression was used to derive hazard ratios (HR, and 95%-confidence intervals). Models included road traffic, railway and aircraft noise, air pollution, and individual and area-level covariates including socio-economic position. Analyses included exposure-response modelling, effect modification, and a subset analysis around airports. The main findings were integrated into meta-analyses with published studies on mortality and incidence (separately and combined). HRs were 1.06 (1.05, 1.07), 1.02 (1.01, 1.03) and 1.01 (0.99, 1.02) per 10 dB day evening-night level (Lden) road traffic, railway and aircraft noise, respectively (adjusted model, including NO2). Splines suggested a threshold for road traffic noise (~ 46 dB Lden, well below the 53 dB Lden WHO guideline level), but not railway noise. Substituting for PM2.5, or including deaths with type 1 DM hardly changed the associations. HRs were higher for males compared to females, and in younger compared to older adults. Focusing only on type 1 DM showed an independent association with road traffic noise. Meta-analysis was only possible for road traffic noise in relation to mortality (1.08 [0.99, 1.18] per 10 dB, n = 4), with the point estimate broadly similar to that for incidence (1.07 [1.05, 1.09] per 10 dB, n = 10). Combining incidence and mortality studies indicated positive associations for each source, strongest for road traffic noise (1.07 [1.05, 1.08], 1.02 [1.01, 1.03], and 1.02 [1.00, 1.03] per 10 dB road traffic [n = 14], railway [n = 5] and aircraft noise [n = 5], respectively). This study provides new evidence that transportation noise is associated with diabetes mortality. With the growing evidence and large disease burden, DM should be viewed as an important outcome in the noise and health discussion.
{"title":"Long-term exposure to transportation noise and diabetes mellitus mortality: a national cohort study and updated meta-analysis","authors":"Danielle Vienneau, Benedikt Wicki, Benjamin Flückiger, Beat Schäffer, Jean Marc Wunderli, Martin Röösli","doi":"10.1186/s12940-024-01084-0","DOIUrl":"https://doi.org/10.1186/s12940-024-01084-0","url":null,"abstract":"Long-term exposure to transportation noise is related to cardio-metabolic diseases, with more recent evidence also showing associations with diabetes mellitus (DM) incidence. This study aimed to evaluate the association between transportation noise and DM mortality within the Swiss National Cohort. During 15 years of follow-up (2001–2015; 4.14 million adults), over 72,000 DM deaths were accrued. Source-specific noise was calculated at residential locations, considering moving history. Multi-exposure, time-varying Cox regression was used to derive hazard ratios (HR, and 95%-confidence intervals). Models included road traffic, railway and aircraft noise, air pollution, and individual and area-level covariates including socio-economic position. Analyses included exposure-response modelling, effect modification, and a subset analysis around airports. The main findings were integrated into meta-analyses with published studies on mortality and incidence (separately and combined). HRs were 1.06 (1.05, 1.07), 1.02 (1.01, 1.03) and 1.01 (0.99, 1.02) per 10 dB day evening-night level (Lden) road traffic, railway and aircraft noise, respectively (adjusted model, including NO2). Splines suggested a threshold for road traffic noise (~ 46 dB Lden, well below the 53 dB Lden WHO guideline level), but not railway noise. Substituting for PM2.5, or including deaths with type 1 DM hardly changed the associations. HRs were higher for males compared to females, and in younger compared to older adults. Focusing only on type 1 DM showed an independent association with road traffic noise. Meta-analysis was only possible for road traffic noise in relation to mortality (1.08 [0.99, 1.18] per 10 dB, n = 4), with the point estimate broadly similar to that for incidence (1.07 [1.05, 1.09] per 10 dB, n = 10). Combining incidence and mortality studies indicated positive associations for each source, strongest for road traffic noise (1.07 [1.05, 1.08], 1.02 [1.01, 1.03], and 1.02 [1.00, 1.03] per 10 dB road traffic [n = 14], railway [n = 5] and aircraft noise [n = 5], respectively). This study provides new evidence that transportation noise is associated with diabetes mortality. With the growing evidence and large disease burden, DM should be viewed as an important outcome in the noise and health discussion.","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":null,"pages":null},"PeriodicalIF":6.0,"publicationDate":"2024-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140837425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-03DOI: 10.1186/s12940-024-01086-y
Ying Wang, Zhaowei Meng, Sen Wei, Xuebing Li, Zheng Su, Yong Jiang, Heng Wu, Hongli Pan, Jing Wang, Qinghua Zhou, Youlin Qiao, Yaguang Fan
Volatile organic compounds (VOCs) encompass hundreds of high production volume chemicals and have been reported to be associated with adverse respiratory outcomes such as chronic obstructive pulmonary disease (COPD). However, research on the combined toxic effects of exposure to various VOCs on COPD is lacking. We aimed to assess the effect of VOC metabolite mixture on COPD risk in a large population sample. We assessed the effect of VOC metabolite mixture on COPD risk in 5997 adults from the National Health and Nutrition Examination Survey (NHANES) from 2011 to 2020 (pre-pandemic) using multivariate logistic regression, Bayesian weighted quantile sum regression (BWQS), quantile-based g-Computation method (Qgcomp), and Bayesian kernel machine regression (BKMR). We explored whether these associations were mediated by white blood cell (WBC) count and total bilirubin. In the logistic regression model, we observed a significantly increased risk of COPD associated with 9 VOC metabolites. Conversely, N-acetyl-S-(benzyl)-L-cysteine (BMA) and N-acetyl-S-(n-propyl)-L-cysteine (BPMA) showed insignificant negative correlations with COPD risk. The overall mixture exposure demonstrated a significant positive relationship with COPD in both the BWQS model (adjusted odds ratio (OR) = 1.30, 95% confidence interval (CI): 1.06, 1.58) and BKMR model, and with marginal significance in the Qgcomp model (adjusted OR = 1.22, 95% CI: 0.98, 1.52). All three models indicated a significant effect of the VOC metabolite mixture on COPD in non-current smokers. WBC count mediated 7.1% of the VOC mixture associated-COPD in non-current smokers. Our findings provide novel evidence suggesting that VOCs may have adverse associations with COPD in the general population, with N, N- Dimethylformamide and 1,3-Butadiene contributing most. These findings underscore the significance of understanding the potential health risks associated with VOC mixture and emphasize the need for targeted interventions to mitigate the adverse effects on COPD risk.
{"title":"Urinary volatile organic compound metabolites and COPD among US adults: mixture, interaction and mediation analysis","authors":"Ying Wang, Zhaowei Meng, Sen Wei, Xuebing Li, Zheng Su, Yong Jiang, Heng Wu, Hongli Pan, Jing Wang, Qinghua Zhou, Youlin Qiao, Yaguang Fan","doi":"10.1186/s12940-024-01086-y","DOIUrl":"https://doi.org/10.1186/s12940-024-01086-y","url":null,"abstract":"Volatile organic compounds (VOCs) encompass hundreds of high production volume chemicals and have been reported to be associated with adverse respiratory outcomes such as chronic obstructive pulmonary disease (COPD). However, research on the combined toxic effects of exposure to various VOCs on COPD is lacking. We aimed to assess the effect of VOC metabolite mixture on COPD risk in a large population sample. We assessed the effect of VOC metabolite mixture on COPD risk in 5997 adults from the National Health and Nutrition Examination Survey (NHANES) from 2011 to 2020 (pre-pandemic) using multivariate logistic regression, Bayesian weighted quantile sum regression (BWQS), quantile-based g-Computation method (Qgcomp), and Bayesian kernel machine regression (BKMR). We explored whether these associations were mediated by white blood cell (WBC) count and total bilirubin. In the logistic regression model, we observed a significantly increased risk of COPD associated with 9 VOC metabolites. Conversely, N-acetyl-S-(benzyl)-L-cysteine (BMA) and N-acetyl-S-(n-propyl)-L-cysteine (BPMA) showed insignificant negative correlations with COPD risk. The overall mixture exposure demonstrated a significant positive relationship with COPD in both the BWQS model (adjusted odds ratio (OR) = 1.30, 95% confidence interval (CI): 1.06, 1.58) and BKMR model, and with marginal significance in the Qgcomp model (adjusted OR = 1.22, 95% CI: 0.98, 1.52). All three models indicated a significant effect of the VOC metabolite mixture on COPD in non-current smokers. WBC count mediated 7.1% of the VOC mixture associated-COPD in non-current smokers. Our findings provide novel evidence suggesting that VOCs may have adverse associations with COPD in the general population, with N, N- Dimethylformamide and 1,3-Butadiene contributing most. These findings underscore the significance of understanding the potential health risks associated with VOC mixture and emphasize the need for targeted interventions to mitigate the adverse effects on COPD risk.","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":null,"pages":null},"PeriodicalIF":6.0,"publicationDate":"2024-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140837406","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-03DOI: 10.1186/s12940-024-01079-x
Novat Pugo Sambodo, Menno Pradhan, Robert Sparrow, Eddy van Doorslaer
The forest fires that ravaged parts of Indonesia in 2015 were the most severely polluting of this century but little is known about their effects on health care utilization of the affected population. We estimate their short-term impact on visit rates to primary and hospital care with particular focus on visits for specific smoke-related conditions (respiratory disease, acute respiratory tract infection (ARTI) and common cold). We estimate the short-term impact of the 2015 forest fire on visit rates to primary and hospital care by combining satellite data on Aerosol Optical Depth (AOD) with administrative records from Indonesian National Health Insurance Agency (BPJS Kesehatan) from January 2015–April 2016. The 16 months of panel data cover 203 districts in the islands of Sumatra and Kalimantan before, during and after the forest fires. We use the (more efficient) ANCOVA version adaptation of a fixed effects model to compare the trends in healthcare use of affected districts (with AOD value above 0.75) with control districts (AOD value below 0.75). Considering the higher vulnerability of children’s lungs, we do this separately for children under 5 and the rest of the population adults (> 5), and for both urban and rural areas, and for both the period during and after the forest fires. We find little effects for adults. For young children we estimate positive effects for care related to respiratory problems in primary health care facilities in urban areas. Hospital care visits in general, on the other hand, are negatively affected in rural areas. We argue that these patterns arise because accessibility of care during fires is more restricted for rural than for urban areas. The severity of the fires and the absence of positive impact on health care utilization for adults and children in rural areas indicate large missed opportunities for receiving necessary care. This is particularly worrisome for children, whose lungs are most vulnerable to the effects. Our findings underscore the need to ensure ongoing access to medical services during forest fires and emphasize the necessity of catching up with essential care for children after the fires, particularly in rural areas.
{"title":"When the smoke gets in your lungs: short-term effects of Indonesia’s 2015 forest fires on health care use","authors":"Novat Pugo Sambodo, Menno Pradhan, Robert Sparrow, Eddy van Doorslaer","doi":"10.1186/s12940-024-01079-x","DOIUrl":"https://doi.org/10.1186/s12940-024-01079-x","url":null,"abstract":"The forest fires that ravaged parts of Indonesia in 2015 were the most severely polluting of this century but little is known about their effects on health care utilization of the affected population. We estimate their short-term impact on visit rates to primary and hospital care with particular focus on visits for specific smoke-related conditions (respiratory disease, acute respiratory tract infection (ARTI) and common cold). We estimate the short-term impact of the 2015 forest fire on visit rates to primary and hospital care by combining satellite data on Aerosol Optical Depth (AOD) with administrative records from Indonesian National Health Insurance Agency (BPJS Kesehatan) from January 2015–April 2016. The 16 months of panel data cover 203 districts in the islands of Sumatra and Kalimantan before, during and after the forest fires. We use the (more efficient) ANCOVA version adaptation of a fixed effects model to compare the trends in healthcare use of affected districts (with AOD value above 0.75) with control districts (AOD value below 0.75). Considering the higher vulnerability of children’s lungs, we do this separately for children under 5 and the rest of the population adults (> 5), and for both urban and rural areas, and for both the period during and after the forest fires. We find little effects for adults. For young children we estimate positive effects for care related to respiratory problems in primary health care facilities in urban areas. Hospital care visits in general, on the other hand, are negatively affected in rural areas. We argue that these patterns arise because accessibility of care during fires is more restricted for rural than for urban areas. The severity of the fires and the absence of positive impact on health care utilization for adults and children in rural areas indicate large missed opportunities for receiving necessary care. This is particularly worrisome for children, whose lungs are most vulnerable to the effects. Our findings underscore the need to ensure ongoing access to medical services during forest fires and emphasize the necessity of catching up with essential care for children after the fires, particularly in rural areas.","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":null,"pages":null},"PeriodicalIF":6.0,"publicationDate":"2024-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140837266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-23DOI: 10.1186/s12940-024-01080-4
David Dillon, C. Ward‐Caviness, Abhijit V. Kshirsagar, J. Moyer, Joel Schwartz, Qian Di, Anne Weaver
{"title":"Associations between long-term exposure to air pollution and kidney function utilizing electronic healthcare records: a cross-sectional study","authors":"David Dillon, C. Ward‐Caviness, Abhijit V. Kshirsagar, J. Moyer, Joel Schwartz, Qian Di, Anne Weaver","doi":"10.1186/s12940-024-01080-4","DOIUrl":"https://doi.org/10.1186/s12940-024-01080-4","url":null,"abstract":"","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":null,"pages":null},"PeriodicalIF":6.0,"publicationDate":"2024-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140667419","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-16DOI: 10.1186/s12940-024-01078-y
Keren Zhang, Kimberly Paul, Jonathan P. Jacobs, Myles G. Cockburn, Jeff M. Bronstein, Irish del Rosario, Beate Ritz
Organophosphorus pesticides (OP) have been associated with various human health conditions. Animal experiments and in-vitro models suggested that OP may also affect the gut microbiota. We examined associations between ambient chronic exposure to OP and gut microbial changes in humans. We recruited 190 participants from a community-based epidemiologic study of Parkinson’s disease living in a region known for heavy agricultural pesticide use in California. Of these, 61% of participants had Parkinson’s disease and their mean age was 72 years. Microbiome and predicted metagenome data were generated by 16S rRNA gene sequencing of fecal samples. Ambient long-term OP exposures were assessed using pesticide application records combined with residential addresses in a geographic information system. We examined gut microbiome differences due to OP exposures, specifically differences in microbial diversity based on the Shannon index and Bray–Curtis dissimilarities, and differential taxa abundance and predicted Metacyc pathway expression relying on regression models and adjusting for potential confounders. OP exposure was not associated with alpha or beta diversity of the gut microbiome. However, the predicted metagenome was sparser and less evenly expressed among those highly exposed to OP (p = 0.04). Additionally, we found that the abundance of two bacterial families, 22 genera, and the predicted expression of 34 Metacyc pathways were associated with long-term OP exposure. These pathways included perturbed processes related to cellular respiration, increased biosynthesis and degradation of compounds related to bacterial wall structure, increased biosynthesis of RNA/DNA precursors, and decreased synthesis of Vitamin B1 and B6. In support of previous animal studies and in-vitro findings, our results suggest that ambient chronic OP pesticide exposure alters gut microbiome composition and its predicted metabolism in humans.
有机磷农药（OP）与人类的各种健康状况有关。动物实验和体外模型表明，OP 也可能影响肠道微生物群。我们研究了环境中长期接触 OP 与人类肠道微生物变化之间的关系。我们从一项基于社区的帕金森病流行病学研究中招募了 190 名参与者，他们居住在加利福尼亚州一个以大量使用农业杀虫剂而闻名的地区。其中，61%的参与者患有帕金森病，他们的平均年龄为 72 岁。通过对粪便样本进行 16S rRNA 基因测序，获得了微生物组和预测的元基因组数据。环境中长期暴露于 OP 的情况是通过地理信息系统中的杀虫剂施用记录与住宅地址相结合进行评估的。我们研究了因暴露于 OP 而导致的肠道微生物组差异，特别是基于香农指数和 Bray-Curtis 差异性的微生物多样性差异、不同类群丰度差异，以及根据回归模型预测的 Metacyc 通路表达，并对潜在的混杂因素进行了调整。OP 暴露与肠道微生物组的α或β多样性无关。然而，在 OP 高暴露人群中，预测的元基因组更稀疏，表达也更不均匀（p = 0.04）。此外，我们还发现，两个细菌科、22 个属的丰度以及 34 种 Metacyc 通路的预测表达与长期暴露于 OP 相关。这些途径包括与细胞呼吸有关的过程受到干扰、与细菌壁结构有关的化合物的生物合成和降解增加、RNA/DNA 前体的生物合成增加以及维生素 B1 和 B6 的合成减少。我们的研究结果表明，环境中长期接触 OP 杀虫剂会改变人类肠道微生物组的组成及其预测的新陈代谢，这与之前的动物研究和体外研究结果相吻合。
{"title":"Ambient long-term exposure to organophosphorus pesticides and the human gut microbiome: an observational study","authors":"Keren Zhang, Kimberly Paul, Jonathan P. Jacobs, Myles G. Cockburn, Jeff M. Bronstein, Irish del Rosario, Beate Ritz","doi":"10.1186/s12940-024-01078-y","DOIUrl":"https://doi.org/10.1186/s12940-024-01078-y","url":null,"abstract":"Organophosphorus pesticides (OP) have been associated with various human health conditions. Animal experiments and in-vitro models suggested that OP may also affect the gut microbiota. We examined associations between ambient chronic exposure to OP and gut microbial changes in humans. We recruited 190 participants from a community-based epidemiologic study of Parkinson’s disease living in a region known for heavy agricultural pesticide use in California. Of these, 61% of participants had Parkinson’s disease and their mean age was 72 years. Microbiome and predicted metagenome data were generated by 16S rRNA gene sequencing of fecal samples. Ambient long-term OP exposures were assessed using pesticide application records combined with residential addresses in a geographic information system. We examined gut microbiome differences due to OP exposures, specifically differences in microbial diversity based on the Shannon index and Bray–Curtis dissimilarities, and differential taxa abundance and predicted Metacyc pathway expression relying on regression models and adjusting for potential confounders. OP exposure was not associated with alpha or beta diversity of the gut microbiome. However, the predicted metagenome was sparser and less evenly expressed among those highly exposed to OP (p = 0.04). Additionally, we found that the abundance of two bacterial families, 22 genera, and the predicted expression of 34 Metacyc pathways were associated with long-term OP exposure. These pathways included perturbed processes related to cellular respiration, increased biosynthesis and degradation of compounds related to bacterial wall structure, increased biosynthesis of RNA/DNA precursors, and decreased synthesis of Vitamin B1 and B6. In support of previous animal studies and in-vitro findings, our results suggest that ambient chronic OP pesticide exposure alters gut microbiome composition and its predicted metabolism in humans.","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":null,"pages":null},"PeriodicalIF":6.0,"publicationDate":"2024-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140581862","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Per- and polyfluoroalkyl substances (PFAS) are associated with many adverse health conditions. Among the main effects is carcinogenicity in humans, which deserves to be further clarified. An evident association has been reported for kidney cancer and testicular cancer. In 2013, a large episode of surface, ground and drinking water contamination with PFAS was uncovered in three provinces of the Veneto Region (northern Italy) involving 30 municipalities and a population of about 150,000. We report on the temporal evolution of all-cause mortality and selected cause-specific mortality by calendar period and birth cohort in the local population between 1980 and 2018. The Italian National Institute of Health pre-processed and made available anonymous data from the Italian National Institute of Statistics death certificate archives for residents of the provinces of Vicenza, Padua and Verona (males, n = 29,629; females, n = 29,518) who died between 1980 and 2018. Calendar period analysis was done by calculating standardised mortality ratios using the total population of the three provinces in the same calendar period as reference. The birth cohort analysis was performed using 20–84 years cumulative standardised mortality ratios. Exposure was defined as being resident in one of the 30 municipalities of the Red area, where the aqueduct supplying drinking water was fed by the contaminated groundwater. During the 34 years between 1985 (assumed as beginning date of water contamination) and 2018 (last year of availability of cause-specific mortality data), in the resident population of the Red area we observed 51,621 deaths vs. 47,731 expected (age- and sex-SMR: 108; 90% CI: 107–109). We found evidence of raised mortality from cardiovascular disease (in particular, heart diseases and ischemic heart disease) and malignant neoplastic diseases, including kidney cancer and testicular cancer. For the first time, an association of PFAS exposure with mortality from cardiovascular disease was formally demonstrated. The evidence regarding kidney cancer and testicular cancer is consistent with previously reported data.
{"title":"All-cause, cardiovascular disease and cancer mortality in the population of a large Italian area contaminated by perfluoroalkyl and polyfluoroalkyl substances (1980–2018)","authors":"Annibale Biggeri, Giorgia Stoppa, Laura Facciolo, Giuliano Fin, Silvia Mancini, Valerio Manno, Giada Minelli, Federica Zamagni, Michela Zamboni, Dolores Catelan, Lauro Bucchi","doi":"10.1186/s12940-024-01074-2","DOIUrl":"https://doi.org/10.1186/s12940-024-01074-2","url":null,"abstract":"Per- and polyfluoroalkyl substances (PFAS) are associated with many adverse health conditions. Among the main effects is carcinogenicity in humans, which deserves to be further clarified. An evident association has been reported for kidney cancer and testicular cancer. In 2013, a large episode of surface, ground and drinking water contamination with PFAS was uncovered in three provinces of the Veneto Region (northern Italy) involving 30 municipalities and a population of about 150,000. We report on the temporal evolution of all-cause mortality and selected cause-specific mortality by calendar period and birth cohort in the local population between 1980 and 2018. The Italian National Institute of Health pre-processed and made available anonymous data from the Italian National Institute of Statistics death certificate archives for residents of the provinces of Vicenza, Padua and Verona (males, n = 29,629; females, n = 29,518) who died between 1980 and 2018. Calendar period analysis was done by calculating standardised mortality ratios using the total population of the three provinces in the same calendar period as reference. The birth cohort analysis was performed using 20–84 years cumulative standardised mortality ratios. Exposure was defined as being resident in one of the 30 municipalities of the Red area, where the aqueduct supplying drinking water was fed by the contaminated groundwater. During the 34 years between 1985 (assumed as beginning date of water contamination) and 2018 (last year of availability of cause-specific mortality data), in the resident population of the Red area we observed 51,621 deaths vs. 47,731 expected (age- and sex-SMR: 108; 90% CI: 107–109). We found evidence of raised mortality from cardiovascular disease (in particular, heart diseases and ischemic heart disease) and malignant neoplastic diseases, including kidney cancer and testicular cancer. For the first time, an association of PFAS exposure with mortality from cardiovascular disease was formally demonstrated. The evidence regarding kidney cancer and testicular cancer is consistent with previously reported data.","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":null,"pages":null},"PeriodicalIF":6.0,"publicationDate":"2024-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140581860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-15DOI: 10.1186/s12940-024-01082-2
Erin L. Landguth, Jonathon Knudson, Jon Graham, Ava Orr, Emily A. Coyle, Paul Smith, Erin O. Semmens, Curtis Noonan
Western Montana, USA, experiences complex air pollution patterns with predominant exposure sources from summer wildfire smoke and winter wood smoke. In addition, climate change related temperatures events are becoming more extreme and expected to contribute to increases in hospital admissions for a range of health outcomes. Evaluating while accounting for these exposures (air pollution and temperature) that often occur simultaneously and may act synergistically on health is becoming more important. We explored short-term exposure to air pollution on children’s respiratory health outcomes and how extreme temperature or seasonal period modify the risk of air pollution-associated healthcare events. The main outcome measure included individual-based address located respiratory-related healthcare visits for three categories: asthma, lower respiratory tract infections (LRTI), and upper respiratory tract infections (URTI) across western Montana for ages 0–17 from 2017–2020. We used a time-stratified, case-crossover analysis with distributed lag models to identify sensitive exposure windows of fine particulate matter (PM2.5) lagged from 0 (same-day) to 14 prior-days modified by temperature or season. For asthma, increases of 1 µg/m3 in PM2.5 exposure 7–13 days prior a healthcare visit date was associated with increased odds that were magnified during median to colder temperatures and winter periods. For LRTIs, 1 µg/m3 increases during 12 days of cumulative PM2.5 with peak exposure periods between 6–12 days before healthcare visit date was associated with elevated LRTI events, also heightened in median to colder temperatures but no seasonal effect was observed. For URTIs, 1 unit increases during 13 days of cumulative PM2.5 with peak exposure periods between 4–10 days prior event date was associated with greater risk for URTIs visits that were intensified during median to hotter temperatures and spring to summer periods. Delayed, short-term exposure increases of PM2.5 were associated with elevated odds of all three pediatric respiratory healthcare visit categories in a sparsely population area of the inter-Rocky Mountains, USA. PM2.5 in colder temperatures tended to increase instances of asthma and LRTIs, while PM2.5 during hotter periods increased URTIs.
{"title":"Seasonal extreme temperatures and short-term fine particulate matter increases pediatric respiratory healthcare encounters in a sparsely populated region of the intermountain western United States","authors":"Erin L. Landguth, Jonathon Knudson, Jon Graham, Ava Orr, Emily A. Coyle, Paul Smith, Erin O. Semmens, Curtis Noonan","doi":"10.1186/s12940-024-01082-2","DOIUrl":"https://doi.org/10.1186/s12940-024-01082-2","url":null,"abstract":"Western Montana, USA, experiences complex air pollution patterns with predominant exposure sources from summer wildfire smoke and winter wood smoke. In addition, climate change related temperatures events are becoming more extreme and expected to contribute to increases in hospital admissions for a range of health outcomes. Evaluating while accounting for these exposures (air pollution and temperature) that often occur simultaneously and may act synergistically on health is becoming more important. We explored short-term exposure to air pollution on children’s respiratory health outcomes and how extreme temperature or seasonal period modify the risk of air pollution-associated healthcare events. The main outcome measure included individual-based address located respiratory-related healthcare visits for three categories: asthma, lower respiratory tract infections (LRTI), and upper respiratory tract infections (URTI) across western Montana for ages 0–17 from 2017–2020. We used a time-stratified, case-crossover analysis with distributed lag models to identify sensitive exposure windows of fine particulate matter (PM2.5) lagged from 0 (same-day) to 14 prior-days modified by temperature or season. For asthma, increases of 1 µg/m3 in PM2.5 exposure 7–13 days prior a healthcare visit date was associated with increased odds that were magnified during median to colder temperatures and winter periods. For LRTIs, 1 µg/m3 increases during 12 days of cumulative PM2.5 with peak exposure periods between 6–12 days before healthcare visit date was associated with elevated LRTI events, also heightened in median to colder temperatures but no seasonal effect was observed. For URTIs, 1 unit increases during 13 days of cumulative PM2.5 with peak exposure periods between 4–10 days prior event date was associated with greater risk for URTIs visits that were intensified during median to hotter temperatures and spring to summer periods. Delayed, short-term exposure increases of PM2.5 were associated with elevated odds of all three pediatric respiratory healthcare visit categories in a sparsely population area of the inter-Rocky Mountains, USA. PM2.5 in colder temperatures tended to increase instances of asthma and LRTIs, while PM2.5 during hotter periods increased URTIs.","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":null,"pages":null},"PeriodicalIF":6.0,"publicationDate":"2024-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140581863","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Per- and polyfluoroalkyl substances (PFAS) are known environmental contaminants with immunosuppressive properties. Their connection to rheumatoid arthritis (RA), a condition influenced by the immune system, is not well studied. This research explores the association between PFAS exposure and RA prevalence. This research utilized data from the NHANES, encompassing a sample of 10,496 adults from the 2003–2018 cycles, focusing on serum levels of several PFAS. The presence of RA was determined based on self-reports. This study used multivariable logistic regression to assess the relationship between individual PFAS and RA risk, adjusting for covariates to calculate odds ratios (ORs). The combined effects of PFAS mixtures were evaluated using BKMR, WQS regression, and quantile g-computation. Additionally, sex-specific associations were explored through stratified analysis. Higher serum PFOA (OR = 0.88, 95% CI: 0.79, 0.98), PFHxS (OR = 0.91, 95% CI: 0.83, 1.00), PFNA (OR = 0.87, 95% CI: 0.77, 0.98), and PFDA (OR = 0.89, 95% CI: 0.81, 0.99) concentration was related to lower odds of RA. Sex-specific analysis in single chemical models indicated the significant inverse associations were only evident in females. BKMR did not show an obvious pattern of RA estimates across PFAS mixture. The outcomes of sex-stratified quantile g-computation demonstrated that an increase in PFAS mixture was associated with a decreased odds of RA in females (OR: 0.76, 95% CI: 0.62, 0.92). We identified a significant interaction term of the WQS*sex in the 100 repeated hold out WQS analysis. Notably, a higher concentration of the PFAS mixture was significantly associated with reduced odds of RA in females (mean OR = 0.93, 95% CI: 0.88, 0.98). This study indicates potential sex-specific associations of exposure to various individual PFAS and their mixtures with RA. Notably, the observed inverse relationships were statistically significant in females but not in males. These findings contribute to the growing body of evidence indicating that PFAS may have immunosuppressive effects.
全氟和多氟烷基物质（PFAS）是已知的具有免疫抑制特性的环境污染物。它们与类风湿性关节炎（RA）（一种受免疫系统影响的疾病）之间的关系尚未得到充分研究。本研究探讨了 PFAS 暴露与 RA 患病率之间的关系。这项研究利用了美国国家健康调查（NHANES）的数据，涵盖了 2003-2018 年期间的 10,496 个成人样本，重点研究了几种全氟辛烷磺酸的血清水平。根据自我报告确定是否患有 RA。本研究采用多变量逻辑回归法评估单个 PFAS 与 RA 风险之间的关系，并对协变量进行调整，计算出几率比（ORs）。使用 BKMR、WQS 回归和量化 g 计算评估了 PFAS 混合物的综合效应。此外，还通过分层分析探讨了性别特异性关联。血清中 PFOA（OR = 0.88，95% CI：0.79，0.98）、PFHxS（OR = 0.91，95% CI：0.83，1.00）、PFNA（OR = 0.87，95% CI：0.77，0.98）和 PFDA（OR = 0.89，95% CI：0.81，0.99）浓度越高，患 RA 的几率越低。在单一化学模型中进行的性别特异性分析表明，显著的反向关联仅在女性中明显。BKMR在PFAS混合物中未显示出明显的RA估计模式。性别分层量化 g 计算的结果表明，PFAS 混合物的增加与女性罹患 RA 的几率降低相关（OR：0.76，95% CI：0.62，0.92）。在 100 次重复保持 WQS 分析中，我们发现了 WQS* 性别的重要交互项。值得注意的是，PFAS 混合物浓度越高，女性患 RA 的几率越低（平均 OR = 0.93，95% CI：0.88, 0.98）。这项研究表明，暴露于各种个别的全氟辛烷磺酸及其混合物与 RA 之间可能存在性别特异性关联。值得注意的是，观察到的反向关系在女性中具有统计学意义，而在男性中则没有。越来越多的证据表明，全氟辛烷磺酸可能具有免疫抑制作用。
{"title":"Associations of per- and polyfluoroalkyl substances (PFAS) and their mixture with risk of rheumatoid arthritis in the U.S. adult population","authors":"Jian-Chao Qiao, Zhen-Hua Li, Yu-Bo Ma, Hui-Ya Ma, Meng-Yue Zhang, Xiu-Jun Zhang, Cheng-Yang Hu","doi":"10.1186/s12940-024-01073-3","DOIUrl":"https://doi.org/10.1186/s12940-024-01073-3","url":null,"abstract":"Per- and polyfluoroalkyl substances (PFAS) are known environmental contaminants with immunosuppressive properties. Their connection to rheumatoid arthritis (RA), a condition influenced by the immune system, is not well studied. This research explores the association between PFAS exposure and RA prevalence. This research utilized data from the NHANES, encompassing a sample of 10,496 adults from the 2003–2018 cycles, focusing on serum levels of several PFAS. The presence of RA was determined based on self-reports. This study used multivariable logistic regression to assess the relationship between individual PFAS and RA risk, adjusting for covariates to calculate odds ratios (ORs). The combined effects of PFAS mixtures were evaluated using BKMR, WQS regression, and quantile g-computation. Additionally, sex-specific associations were explored through stratified analysis. Higher serum PFOA (OR = 0.88, 95% CI: 0.79, 0.98), PFHxS (OR = 0.91, 95% CI: 0.83, 1.00), PFNA (OR = 0.87, 95% CI: 0.77, 0.98), and PFDA (OR = 0.89, 95% CI: 0.81, 0.99) concentration was related to lower odds of RA. Sex-specific analysis in single chemical models indicated the significant inverse associations were only evident in females. BKMR did not show an obvious pattern of RA estimates across PFAS mixture. The outcomes of sex-stratified quantile g-computation demonstrated that an increase in PFAS mixture was associated with a decreased odds of RA in females (OR: 0.76, 95% CI: 0.62, 0.92). We identified a significant interaction term of the WQS*sex in the 100 repeated hold out WQS analysis. Notably, a higher concentration of the PFAS mixture was significantly associated with reduced odds of RA in females (mean OR = 0.93, 95% CI: 0.88, 0.98). This study indicates potential sex-specific associations of exposure to various individual PFAS and their mixtures with RA. Notably, the observed inverse relationships were statistically significant in females but not in males. These findings contribute to the growing body of evidence indicating that PFAS may have immunosuppressive effects.","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":null,"pages":null},"PeriodicalIF":6.0,"publicationDate":"2024-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140586107","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-13DOI: 10.1186/s12940-024-01076-0
Nerea Mourino, Zhuoya Zhang, Mónica Pérez-Ríos, Kimberly Yolton, Bruce P. Lanphear, Aimin Chen, Jessie P. Buckley, Heidi J. Kalkwarf, Kim M. Cecil, Joseph M. Braun
Prenatal or early childhood secondhand tobacco smoke (SHS) exposure increases obesity risk. However, the potential mechanisms underlying this association are unclear, but obesogenic eating behaviors are one pathway that components of SHS could perturb. Our aim was to assess associations of prenatal and early childhood SHS exposure with adolescent eating behaviors. Data came from a prospective pregnancy and birth cohort (N = 207, Cincinnati, OH). With multiple informant models, we estimated associations of prenatal (mean of 16 and 26 weeks of gestation maternal serum cotinine concentrations) and early childhood cotinine (average concentration across ages 12, 24, 36, and 48 months) with eating behaviors at age 12 years (Child Eating Behaviors Questionnaire). We tested whether associations differed by exposure periods and adolescent’s sex. Models adjusted for maternal and child covariates. We found no statistically significant associations between cotinine measures and adolescent’s eating behaviors. Yet, in females, prenatal cotinine was associated with greater food responsiveness (β: 0.23; 95% CI: 0.08, 0.38) and lower satiety responsiveness (β: -0.14; 95% CI: -0.26, -0.02); in males, prenatal and postnatal cotinine was related to lower food responsiveness (prenatal: β: -0.25; 95% CI: -0.04, -0.06; postnatal: β: -0.36; 95% CI: -0.06, -0.11). No significant effect modification by sex or exposure window was found for other eating behaviors. Prenatal and early childhood SHS exposures were not related to adolescent’s eating behavior in this cohort; however, biological sex may modify these associations.
{"title":"Early life exposure to secondhand tobacco smoke and eating behaviors at age 12 years","authors":"Nerea Mourino, Zhuoya Zhang, Mónica Pérez-Ríos, Kimberly Yolton, Bruce P. Lanphear, Aimin Chen, Jessie P. Buckley, Heidi J. Kalkwarf, Kim M. Cecil, Joseph M. Braun","doi":"10.1186/s12940-024-01076-0","DOIUrl":"https://doi.org/10.1186/s12940-024-01076-0","url":null,"abstract":"Prenatal or early childhood secondhand tobacco smoke (SHS) exposure increases obesity risk. However, the potential mechanisms underlying this association are unclear, but obesogenic eating behaviors are one pathway that components of SHS could perturb. Our aim was to assess associations of prenatal and early childhood SHS exposure with adolescent eating behaviors. Data came from a prospective pregnancy and birth cohort (N = 207, Cincinnati, OH). With multiple informant models, we estimated associations of prenatal (mean of 16 and 26 weeks of gestation maternal serum cotinine concentrations) and early childhood cotinine (average concentration across ages 12, 24, 36, and 48 months) with eating behaviors at age 12 years (Child Eating Behaviors Questionnaire). We tested whether associations differed by exposure periods and adolescent’s sex. Models adjusted for maternal and child covariates. We found no statistically significant associations between cotinine measures and adolescent’s eating behaviors. Yet, in females, prenatal cotinine was associated with greater food responsiveness (β: 0.23; 95% CI: 0.08, 0.38) and lower satiety responsiveness (β: -0.14; 95% CI: -0.26, -0.02); in males, prenatal and postnatal cotinine was related to lower food responsiveness (prenatal: β: -0.25; 95% CI: -0.04, -0.06; postnatal: β: -0.36; 95% CI: -0.06, -0.11). No significant effect modification by sex or exposure window was found for other eating behaviors. Prenatal and early childhood SHS exposures were not related to adolescent’s eating behavior in this cohort; however, biological sex may modify these associations.","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":null,"pages":null},"PeriodicalIF":6.0,"publicationDate":"2024-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140586235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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