Pub Date : 2025-11-27DOI: 10.1186/s12940-025-01244-w
Aimée Vester, Yingying Xu, Nicholas C Newman, Melinda C MacDougall, George D Papandonatos, Patrick J Parsons, Christopher D Palmer, Joseph M Braun, Bruce P Lanphear, Aimin Chen, Kim M Cecil, Kimberly Yolton
Background: Lead is a well-known neurotoxicant with no identified safe level. Prior studies found that childhood lead exposure is associated with decreased intelligence quotient (IQ) scores. However, most studies rely on a limited number of blood lead measurements. In this prospective pregnancy and birth cohort, we estimated cumulative childhood lead exposure using repeated blood lead concentrations and regression calibration, allowing for more accurate assessment of lead burden over time and its association with IQ.
Methods: This prospective study included 262 mother-child dyads from Greater Cincinnati enrolled in the Health Outcomes and Measures of the Environment (HOME) Study from 2003 to 2006. We obtained serial blood lead measurements and estimated cumulative childhood lead exposure using a regression calibration method. Outcome was assessed via Wechsler-based IQ testing at ages 5-12 years. We examined the association between estimated cumulative childhood lead exposure and child IQ using linear regression models.
Results: Our cohort had low levels of estimated lifetime average lead exposure (geometric mean: 1.21 μg/dL). Overall, estimated lead exposure decreased from age 12 months to time of IQ test. Cumulative childhood lead exposure estimate was associated with decreased IQ at ages 5-12 years in unadjusted analyses, but not after adjusting for maternal IQ, household income, reported prenatal vitamin use, Home Observation for Measurement of the Environment score, and maternal serum cotinine. Sensitivity analyses additionally adjusting for prenatal total folate did not markedly change our results. We assessed early-life, school-age, or concurrent blood lead exposure estimate in place of cumulative childhood lead exposure estimate and observed a similar pattern of results.
Conclusions: We used a regression calibration method to leverage robust, repeated lead exposure data in our prospective pregnancy and birth cohort. In this cohort with low levels of lead exposure, cumulative childhood lead exposure estimate was negatively associated with school-age IQ in unadjusted analyses but not adjusted analyses. We considered sociodemographic and maternal factors previously associated with cognitive development. Our results suggest these factors may confound the association between low-level child lead exposure and child IQ.
{"title":"Cumulative childhood lead exposure estimation and school-age IQ in a prospective birth cohort.","authors":"Aimée Vester, Yingying Xu, Nicholas C Newman, Melinda C MacDougall, George D Papandonatos, Patrick J Parsons, Christopher D Palmer, Joseph M Braun, Bruce P Lanphear, Aimin Chen, Kim M Cecil, Kimberly Yolton","doi":"10.1186/s12940-025-01244-w","DOIUrl":"10.1186/s12940-025-01244-w","url":null,"abstract":"<p><strong>Background: </strong>Lead is a well-known neurotoxicant with no identified safe level. Prior studies found that childhood lead exposure is associated with decreased intelligence quotient (IQ) scores. However, most studies rely on a limited number of blood lead measurements. In this prospective pregnancy and birth cohort, we estimated cumulative childhood lead exposure using repeated blood lead concentrations and regression calibration, allowing for more accurate assessment of lead burden over time and its association with IQ.</p><p><strong>Methods: </strong>This prospective study included 262 mother-child dyads from Greater Cincinnati enrolled in the Health Outcomes and Measures of the Environment (HOME) Study from 2003 to 2006. We obtained serial blood lead measurements and estimated cumulative childhood lead exposure using a regression calibration method. Outcome was assessed via Wechsler-based IQ testing at ages 5-12 years. We examined the association between estimated cumulative childhood lead exposure and child IQ using linear regression models.</p><p><strong>Results: </strong>Our cohort had low levels of estimated lifetime average lead exposure (geometric mean: 1.21 μg/dL). Overall, estimated lead exposure decreased from age 12 months to time of IQ test. Cumulative childhood lead exposure estimate was associated with decreased IQ at ages 5-12 years in unadjusted analyses, but not after adjusting for maternal IQ, household income, reported prenatal vitamin use, Home Observation for Measurement of the Environment score, and maternal serum cotinine. Sensitivity analyses additionally adjusting for prenatal total folate did not markedly change our results. We assessed early-life, school-age, or concurrent blood lead exposure estimate in place of cumulative childhood lead exposure estimate and observed a similar pattern of results.</p><p><strong>Conclusions: </strong>We used a regression calibration method to leverage robust, repeated lead exposure data in our prospective pregnancy and birth cohort. In this cohort with low levels of lead exposure, cumulative childhood lead exposure estimate was negatively associated with school-age IQ in unadjusted analyses but not adjusted analyses. We considered sociodemographic and maternal factors previously associated with cognitive development. Our results suggest these factors may confound the association between low-level child lead exposure and child IQ.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":" ","pages":"1"},"PeriodicalIF":5.3,"publicationDate":"2025-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12764035/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145631003","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 : 2025-11-17DOI: 10.1186/s12940-025-01239-7
Tuo Liu, Melissa A Furlong, Justin M Snider, Shawn Beitel, Catherine E Mullins, Douglas I Walker, Jaclyn M Goodrich, Derek J Urwin, Jamie Gabriel, Jeff Hughes, John J Gulotta, Miriam M Calkins, Yiwen Liu, Frank A von Hippel, Paloma Beamer, Jefferey L Burgess
<p><strong>Background: </strong>Firefighters have frequent exposure to carcinogens and an increased risk of cancer. Wildland-urban interface (WUI) fires, which involve both structures and undeveloped wildland fuels, pose unique challenges to the health of firefighters. However, the extent of health risks associated with these fires remains underexplored.</p><p><strong>Objectives: </strong>This study aims to identify altered urine metabolites and metabolic processes among male firefighters that were associated with WUI fires as compared with municipal structure fires (MSF).</p><p><strong>Methods: </strong>Untargeted metabolomic profiling was applied to pre-exposure (baseline) and postfire urine samples collected from firefighters responding to WUI and MSF fires. Differential analysis was conducted by fitting linear mixed effects regression models on preprocessed ion intensity and exposure status while adjusting for demographic covariates. Differential metabolites by post-exposure status were identified using a false discovery rate (FDR) threshold of < 0.05. Pathway analysis was performed to identify pathways that were significantly perturbed at a Bonferroni adjusted p-value < 0.05 level. We conducted differential and pathway analyses in both the WUI and MSF cohorts and compared the two fire types in terms of the number of differentially expressed metabolites and patterns of metabolic pathway enrichment.</p><p><strong>Results: </strong>Eighty-five firefighters contributed paired baseline and post-fire samples from WUI events, and 98 firefighters contributed paired baseline and post-fire samples from MSF events. We performed metabolic profiling on baseline and postfire urine samples from WUI and MSF using four modes: HILIC(-), HILIC(+), C18(-), and C18(+) and identified metabolites against an in-house library. We identified 244, 297, 320, and 266 level-1 metabolites from the four respective modes. In the statistical analysis, the main model identified a total of 176 differential metabolites from WUI fires. For MSF, the model identified a total of 652 differential metabolites from the four respective modes. Most metabolites with significant changes after a WUI fire also changed significantly after an MSF event. Two metabolic pathways were significantly enriched after WUI fires, while 7 pathways were significantly enriched after MSF exposure and 2 pathways overlapped between the two types of fires.</p><p><strong>Conclusion: </strong>Fire exposure induces numerous metabolic perturbations in firefighters responding to WUI fires, potentially contributing to their elevated cancer risk. Although individual metabolites changed in a similar fashion across both WUI and MSF, MSF were associated with an increased number of metabolite changes and some of the enriched pathways differed between exposures to WUI fires vs. MSF. These findings suggest that WUI and MSF exposures may share common biological responses while also posing unique health risks to firefighter
{"title":"Evaluating urinary metabolic profiles with wildland-urban-interface (wui) fire exposure among male firefighters: a comparison with municipal structure fires (msf).","authors":"Tuo Liu, Melissa A Furlong, Justin M Snider, Shawn Beitel, Catherine E Mullins, Douglas I Walker, Jaclyn M Goodrich, Derek J Urwin, Jamie Gabriel, Jeff Hughes, John J Gulotta, Miriam M Calkins, Yiwen Liu, Frank A von Hippel, Paloma Beamer, Jefferey L Burgess","doi":"10.1186/s12940-025-01239-7","DOIUrl":"10.1186/s12940-025-01239-7","url":null,"abstract":"<p><strong>Background: </strong>Firefighters have frequent exposure to carcinogens and an increased risk of cancer. Wildland-urban interface (WUI) fires, which involve both structures and undeveloped wildland fuels, pose unique challenges to the health of firefighters. However, the extent of health risks associated with these fires remains underexplored.</p><p><strong>Objectives: </strong>This study aims to identify altered urine metabolites and metabolic processes among male firefighters that were associated with WUI fires as compared with municipal structure fires (MSF).</p><p><strong>Methods: </strong>Untargeted metabolomic profiling was applied to pre-exposure (baseline) and postfire urine samples collected from firefighters responding to WUI and MSF fires. Differential analysis was conducted by fitting linear mixed effects regression models on preprocessed ion intensity and exposure status while adjusting for demographic covariates. Differential metabolites by post-exposure status were identified using a false discovery rate (FDR) threshold of < 0.05. Pathway analysis was performed to identify pathways that were significantly perturbed at a Bonferroni adjusted p-value < 0.05 level. We conducted differential and pathway analyses in both the WUI and MSF cohorts and compared the two fire types in terms of the number of differentially expressed metabolites and patterns of metabolic pathway enrichment.</p><p><strong>Results: </strong>Eighty-five firefighters contributed paired baseline and post-fire samples from WUI events, and 98 firefighters contributed paired baseline and post-fire samples from MSF events. We performed metabolic profiling on baseline and postfire urine samples from WUI and MSF using four modes: HILIC(-), HILIC(+), C18(-), and C18(+) and identified metabolites against an in-house library. We identified 244, 297, 320, and 266 level-1 metabolites from the four respective modes. In the statistical analysis, the main model identified a total of 176 differential metabolites from WUI fires. For MSF, the model identified a total of 652 differential metabolites from the four respective modes. Most metabolites with significant changes after a WUI fire also changed significantly after an MSF event. Two metabolic pathways were significantly enriched after WUI fires, while 7 pathways were significantly enriched after MSF exposure and 2 pathways overlapped between the two types of fires.</p><p><strong>Conclusion: </strong>Fire exposure induces numerous metabolic perturbations in firefighters responding to WUI fires, potentially contributing to their elevated cancer risk. Although individual metabolites changed in a similar fashion across both WUI and MSF, MSF were associated with an increased number of metabolite changes and some of the enriched pathways differed between exposures to WUI fires vs. MSF. These findings suggest that WUI and MSF exposures may share common biological responses while also posing unique health risks to firefighter","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":"24 1","pages":"88"},"PeriodicalIF":5.3,"publicationDate":"2025-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12625405/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145539696","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 : 2025-11-11DOI: 10.1186/s12940-025-01237-9
Adele Carty, Rivka Green, Carly V Goodman, John R McLaughlin, Howard Hu, Bruce Lanphear, E Angeles Martinez-Mier, Amanda J MacFarlane, Gina Muckle, Jeffrey R Brook, Christine Till
Background: The prevalence of autism spectrum disorder has risen in recent decades. Given the growing evidence that prenatal fluoride exposure may be neurotoxic, we examined associations between prenatal fluoride exposure and parent-reported autistic behaviors in preschool-aged children.
Methods: We studied 453 mother-child pairs using data from the Maternal-Infant Research on Environmental Chemicals (MIREC) study, a prospective Canadian birth cohort. Autistic behaviors were assessed in children at 3 to 4 years using the Social Responsiveness Scale-Second Edition (SRS-2) Preschool Form, where a higher score indicates more autistic behaviors. We estimated prenatal fluoride exposure using three methods: (i) maternal urinary fluoride adjusted for specific gravity (MUFSG), from spot urine samples collected at each trimester and the mean calculated across samples, (ii) daily maternal fluoride intake, based on self-reported consumption of tap water, coffee, and tea during the first and third trimesters, and (iii) water fluoride concentration in tap water. We used multivariable linear regression models to estimate associations between the SRS-2 scale T-scores and each fluoride exposure separately. We used multivariable logistic regression to estimate the association between each prenatal fluoride exposure and an elevated SRS-2 total T-score (i.e., 90th percentile or higher). Potential effect modification of MUFSG was examined by child sex, daily folic acid supplementation, and plasma total folate in pregnancy.
Results: The mean SRS-2 total T-score for children aged 3 to 4 years was 45.3 (SD = 6.1, range = 34 to 85). The median MUFSG concentration was 0.43 mg/L (interquartile range = 0.33 mg/L). MUFSG was not significantly associated with the SRS-2 total T-score in multivariable linear regression (β = -0.16; 95% CI, -1.70, 1.39) or logistic regression (OR = 0.76; 95% CI, 0.29, 1.96). Similarly, estimated daily fluoride intake and water fluoride concentration were not associated with the SRS-2 total T-score. No effect modification was observed.
Conclusions: There was no evidence of an association between prenatal fluoride exposure and autistic behaviors in preschool-aged children, in contrast to previous MIREC research findings on lead and phthalates. Given that this cohort has relatively few children with high SRS-2 scores, further research is needed in other groups of children to more fully explore this association.
{"title":"Prenatal fluoride exposure and autistic behaviors in preschool-aged children: the Maternal-Infant Research on Environmental Chemicals (MIREC) cohort study.","authors":"Adele Carty, Rivka Green, Carly V Goodman, John R McLaughlin, Howard Hu, Bruce Lanphear, E Angeles Martinez-Mier, Amanda J MacFarlane, Gina Muckle, Jeffrey R Brook, Christine Till","doi":"10.1186/s12940-025-01237-9","DOIUrl":"10.1186/s12940-025-01237-9","url":null,"abstract":"<p><strong>Background: </strong>The prevalence of autism spectrum disorder has risen in recent decades. Given the growing evidence that prenatal fluoride exposure may be neurotoxic, we examined associations between prenatal fluoride exposure and parent-reported autistic behaviors in preschool-aged children.</p><p><strong>Methods: </strong>We studied 453 mother-child pairs using data from the Maternal-Infant Research on Environmental Chemicals (MIREC) study, a prospective Canadian birth cohort. Autistic behaviors were assessed in children at 3 to 4 years using the Social Responsiveness Scale-Second Edition (SRS-2) Preschool Form, where a higher score indicates more autistic behaviors. We estimated prenatal fluoride exposure using three methods: (i) maternal urinary fluoride adjusted for specific gravity (MUF<sub>SG</sub>), from spot urine samples collected at each trimester and the mean calculated across samples, (ii) daily maternal fluoride intake, based on self-reported consumption of tap water, coffee, and tea during the first and third trimesters, and (iii) water fluoride concentration in tap water. We used multivariable linear regression models to estimate associations between the SRS-2 scale T-scores and each fluoride exposure separately. We used multivariable logistic regression to estimate the association between each prenatal fluoride exposure and an elevated SRS-2 total T-score (i.e., 90th percentile or higher). Potential effect modification of MUF<sub>SG</sub> was examined by child sex, daily folic acid supplementation, and plasma total folate in pregnancy.</p><p><strong>Results: </strong>The mean SRS-2 total T-score for children aged 3 to 4 years was 45.3 (SD = 6.1, range = 34 to 85). The median MUF<sub>SG</sub> concentration was 0.43 mg/L (interquartile range = 0.33 mg/L). MUF<sub>SG</sub> was not significantly associated with the SRS-2 total T-score in multivariable linear regression (β = -0.16; 95% CI, -1.70, 1.39) or logistic regression (OR = 0.76; 95% CI, 0.29, 1.96). Similarly, estimated daily fluoride intake and water fluoride concentration were not associated with the SRS-2 total T-score. No effect modification was observed.</p><p><strong>Conclusions: </strong>There was no evidence of an association between prenatal fluoride exposure and autistic behaviors in preschool-aged children, in contrast to previous MIREC research findings on lead and phthalates. Given that this cohort has relatively few children with high SRS-2 scores, further research is needed in other groups of children to more fully explore this association.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":"24 1","pages":"87"},"PeriodicalIF":5.3,"publicationDate":"2025-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12607120/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145494912","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 : 2025-11-06DOI: 10.1186/s12940-025-01241-z
Adrián David Friedrich, Daniela Belén Gareis, María Eugenia Ordoñez, María Victoria Regge, María Cecilia Santilli, María Natalia Rubinsztain, Mariana Gantov, María Sofía Amarilla, María Eugenia Gaillardou, Carolina Ines Domaica, Mercedes Beatriz Fuertes, Norberto Walter Zwirner
Background: The widespread use of pesticides, including glyphosate-based herbicides (e.g., Roundup®, R) and chlorpyrifos-based insecticides (e.g., Clorpi48®, C), has raised concerns about their environmental and human health impacts. Growing evidence links pesticide exposure to cancer development. Given the critical role of immune surveillance in tumor growth control, environmental pollutants such as pesticides should also be evaluated for immunotoxicity. Moreover, while individual pesticides have been extensively studied, the effects of pesticide mixtures on human immune cells remain poorly explored. Here, we assessed the impact of environmentally relevant doses of R, C, or their combination (R+C) on immune cell functions.
Methods: Peripheral blood mononuclear cells (PBMCs), NK cells, and T cells from healthy donors were exposed to environmentally relevant doses of R, C, or R+C. NK cell cytotoxicity, T-bet expression and IFN-g production were analyzed by flow cytometry, and immune synapse formation (LFA-1 localization) and perforin polarization were analyzed by confocal microscopy. T-cell proliferation, Th1 differentiation, and IL-2 signaling were also evaluated by flow cytometry. Oxidative stress was quantified using a fluorometric assay by measuring H2O2 production in PBMCs exposed to R, C, or R+C. Also, the role of oxidative stress in T-cell dysfunction was assessed.
Results: The combination of R+C, but not the individual compounds, significantly impaired NK cell cytotoxicity, IFN-g production, and immune synapse formation, as evidenced by disrupted LFA-1 localization and defective perforin polarization. In T cells, R+C exposure inhibited proliferation, Th1 differentiation, IL-2 signaling, and IFN-g secretion by CD8⁺ T cells, all key functions for effective antitumor responses. Mechanistically, oxidative stress contributed to the antiproliferative effect, as scavenging of H2O2 by catalase addition restored T cell proliferation.
Conclusions: Environmentally relevant doses of glyphosate and chlorpyrifos-based pesticide mixtures disrupt innate and adaptive immune effector functions that are critical for the control of neoplastic cells and nascent tumor foci, suggesting that current risk assessments underestimate the immunotoxicity of combined formulations.
{"title":"Combined glyphosate and chlorpyrifos-based pesticides impair innate and adaptive immune functions: an in vitro approach.","authors":"Adrián David Friedrich, Daniela Belén Gareis, María Eugenia Ordoñez, María Victoria Regge, María Cecilia Santilli, María Natalia Rubinsztain, Mariana Gantov, María Sofía Amarilla, María Eugenia Gaillardou, Carolina Ines Domaica, Mercedes Beatriz Fuertes, Norberto Walter Zwirner","doi":"10.1186/s12940-025-01241-z","DOIUrl":"10.1186/s12940-025-01241-z","url":null,"abstract":"<p><strong>Background: </strong>The widespread use of pesticides, including glyphosate-based herbicides (e.g., Roundup®, R) and chlorpyrifos-based insecticides (e.g., Clorpi48®, C), has raised concerns about their environmental and human health impacts. Growing evidence links pesticide exposure to cancer development. Given the critical role of immune surveillance in tumor growth control, environmental pollutants such as pesticides should also be evaluated for immunotoxicity. Moreover, while individual pesticides have been extensively studied, the effects of pesticide mixtures on human immune cells remain poorly explored. Here, we assessed the impact of environmentally relevant doses of R, C, or their combination (R+C) on immune cell functions.</p><p><strong>Methods: </strong>Peripheral blood mononuclear cells (PBMCs), NK cells, and T cells from healthy donors were exposed to environmentally relevant doses of R, C, or R+C. NK cell cytotoxicity, T-bet expression and IFN-g production were analyzed by flow cytometry, and immune synapse formation (LFA-1 localization) and perforin polarization were analyzed by confocal microscopy. T-cell proliferation, Th1 differentiation, and IL-2 signaling were also evaluated by flow cytometry. Oxidative stress was quantified using a fluorometric assay by measuring H<sub>2</sub>O<sub>2</sub> production in PBMCs exposed to R, C, or R+C. Also, the role of oxidative stress in T-cell dysfunction was assessed.</p><p><strong>Results: </strong>The combination of R+C, but not the individual compounds, significantly impaired NK cell cytotoxicity, IFN-g production, and immune synapse formation, as evidenced by disrupted LFA-1 localization and defective perforin polarization. In T cells, R+C exposure inhibited proliferation, Th1 differentiation, IL-2 signaling, and IFN-g secretion by CD8⁺ T cells, all key functions for effective antitumor responses. Mechanistically, oxidative stress contributed to the antiproliferative effect, as scavenging of H<sub>2</sub>O<sub>2</sub> by catalase addition restored T cell proliferation.</p><p><strong>Conclusions: </strong>Environmentally relevant doses of glyphosate and chlorpyrifos-based pesticide mixtures disrupt innate and adaptive immune effector functions that are critical for the control of neoplastic cells and nascent tumor foci, suggesting that current risk assessments underestimate the immunotoxicity of combined formulations.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":"24 1","pages":"86"},"PeriodicalIF":5.3,"publicationDate":"2025-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12590857/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145458031","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 : 2025-10-31DOI: 10.1186/s12940-025-01235-x
Durdana Khan, Alexandra Mattia, Zhilin Wang, Ashley J Malin
{"title":"Urinary fluoride and dental fluorosis in relation to kidney and liver function in adolescents and young adults in the United States.","authors":"Durdana Khan, Alexandra Mattia, Zhilin Wang, Ashley J Malin","doi":"10.1186/s12940-025-01235-x","DOIUrl":"10.1186/s12940-025-01235-x","url":null,"abstract":"","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":"24 1","pages":"85"},"PeriodicalIF":5.3,"publicationDate":"2025-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12577127/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145421645","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}
Background: Asbestos is a well-established occupational carcinogen, with strong evidence linking its exposure to lung cancer. Despite increasing awareness of its health risks, asbestos continues to be used in many countries. We aimed to evaluate the global burden of lung cancer attributable to occupational asbestos exposure and to analyze its epidemiological patterns across time and by regions, sex, and age.
Methods: We utilized lung cancer data from the Global Burden of Disease (GBD) 2021 database, including information on new cases, deaths, and disability-adjusted life-years (DALYs), along with their age-standardized rates by gender and age groups. Temporal trends were examined using Joinpoint regression models with 95% confidence intervals (CIs). The timeline data on global asbestos bans were retrieved from the International Ban Asbestos Secretariat.
Results: We observed, approximately 25 years after the complete ban on asbestos use, a declining trend for lung cancer incidence, as well as for mortality and DALYs due to asbestos exposure. In 2021, occupational asbestos exposure accounted for 9.4% of global lung cancer deaths and 7.2% of DALYs. Between 1990 and 2021, the number of asbestos-related lung cancer deaths increased from 0.13 million to 0.19 million, while DALYs rose from 2.58 million to 3.34 million. The highest deaths and DALYs were observed in regions with high Socio-demographic Index (SDI), though the most rapid increases occurred in lower SDI regions. Over time, lung cancer burden shifted towards older populations, especially those aged over 70.
Conclusions: We found, for the first time, that a complete ban on asbestos with a lag time of 25 years could effectively reduce lung cancer incidence along with asbestos-related deaths and DALYs. These findings underscore the urgent need for a complete ban on asbestos (especially chrysotile).
{"title":"Global burden of lung cancer attributable to occupational asbestos exposure: 1990 to 2021.","authors":"Qiulin Huang, Yongran Cheng, Ruijiao Lei, Zijian Chen, Wei Gu, Kari Hemminki, Tianhui Chen","doi":"10.1186/s12940-025-01217-z","DOIUrl":"10.1186/s12940-025-01217-z","url":null,"abstract":"<p><strong>Background: </strong>Asbestos is a well-established occupational carcinogen, with strong evidence linking its exposure to lung cancer. Despite increasing awareness of its health risks, asbestos continues to be used in many countries. We aimed to evaluate the global burden of lung cancer attributable to occupational asbestos exposure and to analyze its epidemiological patterns across time and by regions, sex, and age.</p><p><strong>Methods: </strong>We utilized lung cancer data from the Global Burden of Disease (GBD) 2021 database, including information on new cases, deaths, and disability-adjusted life-years (DALYs), along with their age-standardized rates by gender and age groups. Temporal trends were examined using Joinpoint regression models with 95% confidence intervals (CIs). The timeline data on global asbestos bans were retrieved from the International Ban Asbestos Secretariat.</p><p><strong>Results: </strong>We observed, approximately 25 years after the complete ban on asbestos use, a declining trend for lung cancer incidence, as well as for mortality and DALYs due to asbestos exposure. In 2021, occupational asbestos exposure accounted for 9.4% of global lung cancer deaths and 7.2% of DALYs. Between 1990 and 2021, the number of asbestos-related lung cancer deaths increased from 0.13 million to 0.19 million, while DALYs rose from 2.58 million to 3.34 million. The highest deaths and DALYs were observed in regions with high Socio-demographic Index (SDI), though the most rapid increases occurred in lower SDI regions. Over time, lung cancer burden shifted towards older populations, especially those aged over 70.</p><p><strong>Conclusions: </strong>We found, for the first time, that a complete ban on asbestos with a lag time of 25 years could effectively reduce lung cancer incidence along with asbestos-related deaths and DALYs. These findings underscore the urgent need for a complete ban on asbestos (especially chrysotile).</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":"24 1","pages":"84"},"PeriodicalIF":5.3,"publicationDate":"2025-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12573932/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145408495","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 : 2025-10-27DOI: 10.1186/s12940-025-01224-0
Elisabeth Castillo, Sunil Khanna, Taylor Vogel, Julie Herbstman, Diana Rohlman
{"title":"Not whether but how: the ethics and Language of reporting back individual results.","authors":"Elisabeth Castillo, Sunil Khanna, Taylor Vogel, Julie Herbstman, Diana Rohlman","doi":"10.1186/s12940-025-01224-0","DOIUrl":"10.1186/s12940-025-01224-0","url":null,"abstract":"","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":"24 1","pages":"83"},"PeriodicalIF":5.3,"publicationDate":"2025-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12560451/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145376393","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 : 2025-10-27DOI: 10.1186/s12940-025-01232-0
Pierluigi Cocco, Federico Meloni, Carlotta Trobbiani, Lucia Miligi, Daniela Ferrante, Marina Padoan, Giovanni Maria Ferri, Angela Gambelunghe, Giacomo Muzi, Corrado Magnani, Angelo Palmas, Giovanna Piras, Sara Piro, Mariagrazia Zucca, Maria Grazia Ennas, Roberta Zanotti, Aldo Scarpa, Sara De Matteis
{"title":"Occupational exposure to formaldehyde and risk of lymphoma subtypes: results of a multicentre Italian case-control study.","authors":"Pierluigi Cocco, Federico Meloni, Carlotta Trobbiani, Lucia Miligi, Daniela Ferrante, Marina Padoan, Giovanni Maria Ferri, Angela Gambelunghe, Giacomo Muzi, Corrado Magnani, Angelo Palmas, Giovanna Piras, Sara Piro, Mariagrazia Zucca, Maria Grazia Ennas, Roberta Zanotti, Aldo Scarpa, Sara De Matteis","doi":"10.1186/s12940-025-01232-0","DOIUrl":"10.1186/s12940-025-01232-0","url":null,"abstract":"","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":"24 1","pages":"82"},"PeriodicalIF":5.3,"publicationDate":"2025-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12557863/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145376441","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 : 2025-10-24DOI: 10.1186/s12940-025-01218-y
Kate Li, Karin Ricker, Feng C Tsai, Vanessa Cheng, Gwendolyn Osborne, Neela Guha, Sarah Elmore, Isabel Alvarado-Cruz, Martha S Sandy, Meng Sun
{"title":"Carcinogenicity of vinyl acetate: evidence from multiple data streams.","authors":"Kate Li, Karin Ricker, Feng C Tsai, Vanessa Cheng, Gwendolyn Osborne, Neela Guha, Sarah Elmore, Isabel Alvarado-Cruz, Martha S Sandy, Meng Sun","doi":"10.1186/s12940-025-01218-y","DOIUrl":"10.1186/s12940-025-01218-y","url":null,"abstract":"","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":"24 1","pages":"81"},"PeriodicalIF":5.3,"publicationDate":"2025-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12551282/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145367893","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 : 2025-10-22DOI: 10.1186/s12940-025-01227-x
Aurélie M N Danjou, Antoine Lafontaine, Bénédicte Jacquemin, Danielle Vienneau, Kees de Hoogh, Laure Faure, Jacqueline Clavel, Stéphanie Goujon
{"title":"Traffic-related air pollution exposure at birth and risk of childhood leukemia: results from the GEOCAP-Birth case-control study.","authors":"Aurélie M N Danjou, Antoine Lafontaine, Bénédicte Jacquemin, Danielle Vienneau, Kees de Hoogh, Laure Faure, Jacqueline Clavel, Stéphanie Goujon","doi":"10.1186/s12940-025-01227-x","DOIUrl":"10.1186/s12940-025-01227-x","url":null,"abstract":"","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":"24 1","pages":"80"},"PeriodicalIF":5.3,"publicationDate":"2025-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12541972/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145344257","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}
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