Groundwater arsenic poisoning has posed serious health hazards in the exposed population. The objective of the study is to evaluate the arsenic ingestion from breastmilk among pediatric population in Bihar. In the present study, the total women selected were n = 513. Out of which n = 378 women after consent provided their breastmilk for the study, n = 58 subjects were non-lactating but had some type of disease in them and n = 77 subjects denied for the breastmilk sample. Hence, they were selected for the women health study. In addition, urine samples from n = 184 infants' urine were collected for human arsenic exposure study. The study reveals that the arsenic content in the exposed women (in 55%) was significantly high in the breast milk against the WHO permissible limit 0.64 µg/L followed by their urine and blood samples as biological marker. Moreover, the child's urine also had arsenic content greater than the permissible limit (< 50 µg/L) in 67% of the studied children from the arsenic exposed regions. Concerningly, the rate at which arsenic is eliminated from an infant's body via urine in real time was only 50%. This arsenic exposure to young infants has caused potential risks and future health implications. Moreover, the arsenic content was also very high in the analyzed staple food samples such as rice, wheat and potato which is the major cause for arsenic contamination in breastmilk. The study advocates for prompt action to address the issue and implement stringent legislative measures in order to mitigate and eradicate this pressing problem that has implications for future generations.
{"title":"High arsenic contamination in the breast milk of mothers inhabiting the Gangetic plains of Bihar: a major health risk to infants.","authors":"Arun Kumar, Radhika Agarwal, Kanhaiya Kumar, Nirmal Kumar Chayal, Mohammad Ali, Abhinav Srivastava, Mukesh Kumar, Pintoo Kumar Niraj, Siddhant Aryal, Dhruv Kumar, Akhouri Bishwapriya, Shreya Singh, Tejasvi Pandey, Kumar Sambhav Verma, Santosh Kumar, Manisha Singh, Ashok Kumar Ghosh","doi":"10.1186/s12940-024-01115-w","DOIUrl":"https://doi.org/10.1186/s12940-024-01115-w","url":null,"abstract":"<p><p>Groundwater arsenic poisoning has posed serious health hazards in the exposed population. The objective of the study is to evaluate the arsenic ingestion from breastmilk among pediatric population in Bihar. In the present study, the total women selected were n = 513. Out of which n = 378 women after consent provided their breastmilk for the study, n = 58 subjects were non-lactating but had some type of disease in them and n = 77 subjects denied for the breastmilk sample. Hence, they were selected for the women health study. In addition, urine samples from n = 184 infants' urine were collected for human arsenic exposure study. The study reveals that the arsenic content in the exposed women (in 55%) was significantly high in the breast milk against the WHO permissible limit 0.64 µg/L followed by their urine and blood samples as biological marker. Moreover, the child's urine also had arsenic content greater than the permissible limit (< 50 µg/L) in 67% of the studied children from the arsenic exposed regions. Concerningly, the rate at which arsenic is eliminated from an infant's body via urine in real time was only 50%. This arsenic exposure to young infants has caused potential risks and future health implications. Moreover, the arsenic content was also very high in the analyzed staple food samples such as rice, wheat and potato which is the major cause for arsenic contamination in breastmilk. The study advocates for prompt action to address the issue and implement stringent legislative measures in order to mitigate and eradicate this pressing problem that has implications for future generations.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11415992/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142282265","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 : 2024-09-19DOI: 10.1186/s12940-024-01114-x
Jack Rubinstein, Susan M. Pinney, Changchun Xie, Hong-Sheng Wang
Exposure to phenols has been linked in animal models and human populations to cardiac function alterations and cardiovascular diseases, although their effects on cardiac electrical properties in humans remains to be established. This study aimed to identify changes in electrocardiographic (ECG) parameters associated with environmental phenol exposure in adults of a midwestern large cohort known as the Fernald Community Cohort (FCC). During the day of the first comprehensive medical examination, urine samples were obtained, and electrocardiograms were recorded. Cross-sectional linear regression analyses were performed. Bisphenol A (BPA) and bisphenol F (BPF) were both associated with a longer PR interval, an indication of delayed atrial-to-ventricle conduction, in females (p < 0.05) but not males. BPA combined with BPF was associated with an increase QRS duration, an indication of delayed ventricular activation, in females (P < 0.05) but not males. Higher triclocarban (TCC) level was associated with longer QTc interval, an indication of delayed ventricular repolarization, in males (P < 0.01) but not females. Body mass index (BMI) was associated with a significant increase in PR and QTc intervals and ventricular rate in females and in ventricular rate in males. In females, the combined effect of being in the top tertile for both BPA urinary concentration and BMI was an estimate of a 10% increase in PR interval. No associations were found with the other phenols. Higher exposure to some phenols was associated with alterations of cardiac electrical properties in a sex specific manner in the Fernald cohort. Our population-based findings correlate directly with clinically relevant parameters that are associated with known pathophysiologic cardiac conditions in humans.
{"title":"Association of same-day urinary phenol levels and cardiac electrical alterations: analysis of the Fernald Community Cohort","authors":"Jack Rubinstein, Susan M. Pinney, Changchun Xie, Hong-Sheng Wang","doi":"10.1186/s12940-024-01114-x","DOIUrl":"https://doi.org/10.1186/s12940-024-01114-x","url":null,"abstract":"Exposure to phenols has been linked in animal models and human populations to cardiac function alterations and cardiovascular diseases, although their effects on cardiac electrical properties in humans remains to be established. This study aimed to identify changes in electrocardiographic (ECG) parameters associated with environmental phenol exposure in adults of a midwestern large cohort known as the Fernald Community Cohort (FCC). During the day of the first comprehensive medical examination, urine samples were obtained, and electrocardiograms were recorded. Cross-sectional linear regression analyses were performed. Bisphenol A (BPA) and bisphenol F (BPF) were both associated with a longer PR interval, an indication of delayed atrial-to-ventricle conduction, in females (p < 0.05) but not males. BPA combined with BPF was associated with an increase QRS duration, an indication of delayed ventricular activation, in females (P < 0.05) but not males. Higher triclocarban (TCC) level was associated with longer QTc interval, an indication of delayed ventricular repolarization, in males (P < 0.01) but not females. Body mass index (BMI) was associated with a significant increase in PR and QTc intervals and ventricular rate in females and in ventricular rate in males. In females, the combined effect of being in the top tertile for both BPA urinary concentration and BMI was an estimate of a 10% increase in PR interval. No associations were found with the other phenols. Higher exposure to some phenols was associated with alterations of cardiac electrical properties in a sex specific manner in the Fernald cohort. Our population-based findings correlate directly with clinically relevant parameters that are associated with known pathophysiologic cardiac conditions in humans.","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":null,"pages":null},"PeriodicalIF":6.0,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142252510","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 : 2024-09-17DOI: 10.1186/s12940-024-01111-0
Gerard Hoek, Danielle Vienneau, Kees de Hoogh
Epidemiological studies of long-term exposure to outdoor air pollution have consistently documented associations with morbidity and mortality. Air pollution exposure in these epidemiological studies is generally assessed at the residential address, because individual time-activity patterns are seldom known in large epidemiological studies. Ignoring time-activity patterns may result in bias in epidemiological studies. The aims of this paper are to assess the agreement between exposure assessed at the residential address and exposures estimated with time-activity integrated and the potential bias in epidemiological studies when exposure is estimated at the residential address. We reviewed exposure studies that have compared residential and time-activity integrated exposures, with a focus on the correlation. We further discuss epidemiological studies that have compared health effect estimates between the residential and time-activity integrated exposure and studies that have indirectly estimated the potential bias in health effect estimates in epidemiological studies related to ignoring time-activity patterns. A large number of studies compared residential and time-activity integrated exposure, especially in Europe and North America, mostly focusing on differences in level. Eleven of these studies reported correlations, showing that the correlation between residential address-based and time-activity integrated long-term air pollution exposure was generally high to very high (R > 0.8). For individual subjects large differences were found between residential and time-activity integrated exposures. Consistent with the high correlation, five of six identified epidemiological studies found nearly identical health effects using residential and time-activity integrated exposure. Six additional studies in Europe and North America showed only small to moderate potential bias (9 to 30% potential underestimation) in estimated exposure response functions using residence-based exposures. Differences of average exposure level were generally small and in both directions. Exposure contrasts were smaller for time-activity integrated exposures in nearly all studies. The difference in exposure was not equally distributed across the population including between different socio-economic groups. Overall, the bias in epidemiological studies related to assessing long-term exposure at the residential address only is likely small in populations comparable to those evaluated in the comparison studies. Further improvements in exposure assessment especially for large populations remain useful.
{"title":"Does residential address-based exposure assessment for outdoor air pollution lead to bias in epidemiological studies?","authors":"Gerard Hoek, Danielle Vienneau, Kees de Hoogh","doi":"10.1186/s12940-024-01111-0","DOIUrl":"https://doi.org/10.1186/s12940-024-01111-0","url":null,"abstract":"Epidemiological studies of long-term exposure to outdoor air pollution have consistently documented associations with morbidity and mortality. Air pollution exposure in these epidemiological studies is generally assessed at the residential address, because individual time-activity patterns are seldom known in large epidemiological studies. Ignoring time-activity patterns may result in bias in epidemiological studies. The aims of this paper are to assess the agreement between exposure assessed at the residential address and exposures estimated with time-activity integrated and the potential bias in epidemiological studies when exposure is estimated at the residential address. We reviewed exposure studies that have compared residential and time-activity integrated exposures, with a focus on the correlation. We further discuss epidemiological studies that have compared health effect estimates between the residential and time-activity integrated exposure and studies that have indirectly estimated the potential bias in health effect estimates in epidemiological studies related to ignoring time-activity patterns. A large number of studies compared residential and time-activity integrated exposure, especially in Europe and North America, mostly focusing on differences in level. Eleven of these studies reported correlations, showing that the correlation between residential address-based and time-activity integrated long-term air pollution exposure was generally high to very high (R > 0.8). For individual subjects large differences were found between residential and time-activity integrated exposures. Consistent with the high correlation, five of six identified epidemiological studies found nearly identical health effects using residential and time-activity integrated exposure. Six additional studies in Europe and North America showed only small to moderate potential bias (9 to 30% potential underestimation) in estimated exposure response functions using residence-based exposures. Differences of average exposure level were generally small and in both directions. Exposure contrasts were smaller for time-activity integrated exposures in nearly all studies. The difference in exposure was not equally distributed across the population including between different socio-economic groups. Overall, the bias in epidemiological studies related to assessing long-term exposure at the residential address only is likely small in populations comparable to those evaluated in the comparison studies. Further improvements in exposure assessment especially for large populations remain useful.","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":null,"pages":null},"PeriodicalIF":6.0,"publicationDate":"2024-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142252511","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 : 2024-09-12DOI: 10.1186/s12940-024-01113-y
Nathan B. Morris, Nicholas Ravanelli, Georgia K. Chaseling
Ethyl alcohol (ethanol) consumption is ostensibly known to increase the risk of morbidity and mortality during hot weather and heatwaves. However, how alcohol independently alters physiological, perceptual, and behavioral responses to heat stress remains poorly understood. Therefore, we conducted a systematic scoping review to understand how alcohol consumption affects thermoregulatory responses to the heat. We searched five databases employing the following eligibility criteria, studies must have: 1) involved the oral consumption of ethanol, 2) employed a randomized or crossover-control study design with a control trial consisting of a volume-matched, non-alcoholic beverage, 3) been conducted in healthy adult humans, 4) reported thermophysiological, perceptual, hydration status markers, and/or behavioral outcomes, 5) been published in English, 6) been conducted in air or water at temperatures of > 28°C, 7) involved passive rest or exercise, and 8) been published before October 4th, 2023. After removing duplicates, 7256 titles were screened, 29 papers were assessed for eligibility and 8 papers were included in the final review. Across the 8 studies, there were a total of 93 participants (93 male/0 female), the average time of heat exposure was 70 min and average alcohol dose was 0.68 g·kg1. There were 23 unique outcome variables analyzed from the studies. The physiological marker most influenced by alcohol was core temperature (lowered with alcohol consumption in 3/4 studies). Additionally, skin blood flow was increased with alcohol consumption in the one study that measured it. Typical markers of dehydration, such as increased urine volume (1/3 studies), mass loss (1/3 studies) and decreased plasma volume (0/2 studies) were not consistently observed in these studies, except for in the study with the highest alcohol dose. The effect of alcohol consumption on thermoregulatory responses is understudied, and is limited by moderate doses of alcohol consumption, short durations of heat exposure, and only conducted in young-healthy males. Contrary to current heat-health advice, the available literature suggests that alcohol consumption does not seem to impair physiological responses to heat in young healthy males.
{"title":"The effect of alcohol consumption on human physiological and perceptual responses to heat stress: a systematic scoping review","authors":"Nathan B. Morris, Nicholas Ravanelli, Georgia K. Chaseling","doi":"10.1186/s12940-024-01113-y","DOIUrl":"https://doi.org/10.1186/s12940-024-01113-y","url":null,"abstract":"Ethyl alcohol (ethanol) consumption is ostensibly known to increase the risk of morbidity and mortality during hot weather and heatwaves. However, how alcohol independently alters physiological, perceptual, and behavioral responses to heat stress remains poorly understood. Therefore, we conducted a systematic scoping review to understand how alcohol consumption affects thermoregulatory responses to the heat. We searched five databases employing the following eligibility criteria, studies must have: 1) involved the oral consumption of ethanol, 2) employed a randomized or crossover-control study design with a control trial consisting of a volume-matched, non-alcoholic beverage, 3) been conducted in healthy adult humans, 4) reported thermophysiological, perceptual, hydration status markers, and/or behavioral outcomes, 5) been published in English, 6) been conducted in air or water at temperatures of > 28°C, 7) involved passive rest or exercise, and 8) been published before October 4th, 2023. After removing duplicates, 7256 titles were screened, 29 papers were assessed for eligibility and 8 papers were included in the final review. Across the 8 studies, there were a total of 93 participants (93 male/0 female), the average time of heat exposure was 70 min and average alcohol dose was 0.68 g·kg1. There were 23 unique outcome variables analyzed from the studies. The physiological marker most influenced by alcohol was core temperature (lowered with alcohol consumption in 3/4 studies). Additionally, skin blood flow was increased with alcohol consumption in the one study that measured it. Typical markers of dehydration, such as increased urine volume (1/3 studies), mass loss (1/3 studies) and decreased plasma volume (0/2 studies) were not consistently observed in these studies, except for in the study with the highest alcohol dose. The effect of alcohol consumption on thermoregulatory responses is understudied, and is limited by moderate doses of alcohol consumption, short durations of heat exposure, and only conducted in young-healthy males. Contrary to current heat-health advice, the available literature suggests that alcohol consumption does not seem to impair physiological responses to heat in young healthy males.","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":null,"pages":null},"PeriodicalIF":6.0,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142186506","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 : 2024-09-12DOI: 10.1186/s12940-024-01112-z
Marnie F. Hazlehurst, Anjum Hajat, Pooja S. Tandon, Adam A. Szpiro, Joel D. Kaufman, Frances A. Tylavsky, Marion E. Hare, Sheela Sathyanarayana, Christine T. Loftus, Kaja Z. LeWinn, Nicole R. Bush, Catherine J. Karr
<p><b>Correction: Environ Health 23, 17 (2024)</b></p><p><b>https://doi.org/10.1186/s12940-024-01051-9</b></p><p>Following publication of the original article [1], the authors identified an error in Table 5. In the PDF version, Table 5, there were missing data.</p><p>The correct table is provided below and the original article has been updated.</p><figure><figcaption><b data-test="table-caption">Table 1</b></figcaption><span>Full size table</span><svg aria-hidden="true" focusable="false" height="16" role="img" width="16"><use xlink:href="#icon-eds-i-chevron-right-small" xmlns:xlink="http://www.w3.org/1999/xlink"></use></svg></figure><ol data-track-component="outbound reference" data-track-context="references section"><li data-counter="1."><p>Hazlehurst MF, Hajat A, Tandon PS, et al. Associations of residential green space with internalizing and externalizing behavior in early childhood. Environ Health. 2024;23:17. https://doi.org/10.1186/s12940-024-01051-9.</p><p>Article Google Scholar </p></li></ol><p>Download references<svg aria-hidden="true" focusable="false" height="16" role="img" width="16"><use xlink:href="#icon-eds-i-download-medium" xmlns:xlink="http://www.w3.org/1999/xlink"></use></svg></p><h3>Authors and Affiliations</h3><ol><li><p>Department of Epidemiology, Department of Environmental & Occupational Health Sciences, University of Washington School of Public Health, 4225 Roosevelt Way NE, Seattle, WA, 98105, USA</p><p>Marnie F. Hazlehurst</p></li><li><p>Department of Epidemiology, University of Washington School of Public Health, Seattle, WA, USA</p><p>Anjum Hajat</p></li><li><p>Seattle Children’s Research Institute, Department of Pediatrics, University of Washington School of Medicine, Seattle, WA, USA</p><p>Pooja S. Tandon</p></li><li><p>Department of Biostatistics, University of Washington School of Public Health, Seattle, WA, USA</p><p>Adam A. Szpiro</p></li><li><p>Department of Environmental & Occupational Health Sciences, Department of Epidemiology, Division of General Internal Medicine, Department of Medicine, University of Washington School of Public Health, University of Washington School of Medicine, Seattle, WA, USA</p><p>Joel D. Kaufman</p></li><li><p>Department of Preventive Medicine, University of Tennessee Health Science Center, Memphis, TN, USA</p><p>Frances A. Tylavsky & Marion E. Hare</p></li><li><p>Seattle Children’s Research Institute; Department of Pediatrics, University of Washington School of Medicine; Department of Environmental & Occupational Health Sciences, University of Washington School of Public Health, Seattle, WA, USA</p><p>Sheela Sathyanarayana</p></li><li><p>Department of Environmental & Occupational Health Sciences, University of Washington School of Public Health, Seattle, WA, USA</p><p>Christine T. Loftus</p></li><li><p>Department of Psychiatry School of Medicine, University of California San Francisco, San Francisco, CA, USA</p><p>Kaja Z. LeWinn</p></li><li><p>Department of Psyc
0/）适用于本文提供的数据，除非在数据的贷方栏中另有说明。转载与授权引用本文Hazlehurst, M.F., Hajat, A., Tandon, P.S. et al. Correction：住宅绿地与幼儿期内化和外化行为的关系》。Environ Health 23, 74 (2024). https://doi.org/10.1186/s12940-024-01112-zDownload citationPublished: 12 September 2024DOI: https://doi.org/10.1186/s12940-024-01112-zShare this articleAnyone you share the following link with will be able to read this content:Get shareable linkSorry, a shareable link is not currently available for this article.Copy to clipboard Provided by the Springer Nature SharedIt content-sharing initiative
{"title":"Correction: Associations of residential green space with internalizing and externalizing behavior in early childhood","authors":"Marnie F. Hazlehurst, Anjum Hajat, Pooja S. Tandon, Adam A. Szpiro, Joel D. Kaufman, Frances A. Tylavsky, Marion E. Hare, Sheela Sathyanarayana, Christine T. Loftus, Kaja Z. LeWinn, Nicole R. Bush, Catherine J. Karr","doi":"10.1186/s12940-024-01112-z","DOIUrl":"https://doi.org/10.1186/s12940-024-01112-z","url":null,"abstract":"<p><b>Correction: Environ Health 23, 17 (2024)</b></p><p><b>https://doi.org/10.1186/s12940-024-01051-9</b></p><p>Following publication of the original article [1], the authors identified an error in Table 5. In the PDF version, Table 5, there were missing data.</p><p>The correct table is provided below and the original article has been updated.</p><figure><figcaption><b data-test=\"table-caption\">Table 1</b></figcaption><span>Full size table</span><svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"><use xlink:href=\"#icon-eds-i-chevron-right-small\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"></use></svg></figure><ol data-track-component=\"outbound reference\" data-track-context=\"references section\"><li data-counter=\"1.\"><p>Hazlehurst MF, Hajat A, Tandon PS, et al. Associations of residential green space with internalizing and externalizing behavior in early childhood. Environ Health. 2024;23:17. https://doi.org/10.1186/s12940-024-01051-9.</p><p>Article Google Scholar </p></li></ol><p>Download references<svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"><use xlink:href=\"#icon-eds-i-download-medium\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"></use></svg></p><h3>Authors and Affiliations</h3><ol><li><p>Department of Epidemiology, Department of Environmental & Occupational Health Sciences, University of Washington School of Public Health, 4225 Roosevelt Way NE, Seattle, WA, 98105, USA</p><p>Marnie F. Hazlehurst</p></li><li><p>Department of Epidemiology, University of Washington School of Public Health, Seattle, WA, USA</p><p>Anjum Hajat</p></li><li><p>Seattle Children’s Research Institute, Department of Pediatrics, University of Washington School of Medicine, Seattle, WA, USA</p><p>Pooja S. Tandon</p></li><li><p>Department of Biostatistics, University of Washington School of Public Health, Seattle, WA, USA</p><p>Adam A. Szpiro</p></li><li><p>Department of Environmental & Occupational Health Sciences, Department of Epidemiology, Division of General Internal Medicine, Department of Medicine, University of Washington School of Public Health, University of Washington School of Medicine, Seattle, WA, USA</p><p>Joel D. Kaufman</p></li><li><p>Department of Preventive Medicine, University of Tennessee Health Science Center, Memphis, TN, USA</p><p>Frances A. Tylavsky & Marion E. Hare</p></li><li><p>Seattle Children’s Research Institute; Department of Pediatrics, University of Washington School of Medicine; Department of Environmental & Occupational Health Sciences, University of Washington School of Public Health, Seattle, WA, USA</p><p>Sheela Sathyanarayana</p></li><li><p>Department of Environmental & Occupational Health Sciences, University of Washington School of Public Health, Seattle, WA, USA</p><p>Christine T. Loftus</p></li><li><p>Department of Psychiatry School of Medicine, University of California San Francisco, San Francisco, CA, USA</p><p>Kaja Z. LeWinn</p></li><li><p>Department of Psyc","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":null,"pages":null},"PeriodicalIF":6.0,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142186505","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}
Background: While genetic, hormonal, and lifestyle factors partially elucidate the incidence of breast cancer, emerging research has underscored the potential contribution of air pollution. Polychlorinated biphenyls (PCBs) and benzo[a]pyrene (BaP) are of particular concern due to endocrine-disrupting properties and their carcinogenetic effect.
Objective: To identify distinct long term trajectories of exposure to PCB153 and BaP, and estimate their associations with breast cancer risk.
Methods: We used data from the XENAIR case-control study, nested within the ongoing prospective French E3N cohort which enrolled 98,995 women aged 40-65 years in 1990-1991. Cases were incident cases of primary invasive breast cancer diagnosed from cohort entry to 2011. Controls were randomly selected by incidence density sampling, and individually matched to cases on delay since cohort entry, and date, age, department of residence, and menopausal status at cohort entry. Annual mean outdoor PCB153 and BaP concentrations at residential addresses from 1990 to 2011 were estimated using the CHIMERE chemistry-transport model. Latent class mixed models were used to identify profiles of exposure trajectories from cohort entry to the index date, and conditional logistic regression to estimate their association with the odds of breast cancer.
Results: 5058 cases and 5059 controls contributed to the analysis. Five profiles of trajectories of PCB153 exposure were identified. The class with the highest PCB153 concentrations had a 69% increased odds of breast cancer compared to the class with the lowest concentrations (95% CI 1.08, 2.64), after adjustment for education and matching factors. The association between identified BaP trajectories and breast cancer was weaker and suffered from large CI.
Conclusions: Our results support an association between long term exposure to PCB153 and the risk of breast cancer, and encourage further studies to account for lifetime exposure to persistent organic pollutants.
{"title":"Trajectories of long-term exposure to PCB153 and Benzo[a]pyrene (BaP) air pollution and risk of breast cancer.","authors":"Pauline Desnavailles, Delphine Praud, Blandine Le Provost, Hidetaka Kobayashi, Floriane Deygas, Amina Amadou, Thomas Coudon, Lény Grassot, Elodie Faure, Florian Couvidat, Gianluca Severi, Francesca Romana Mancini, Béatrice Fervers, Cécile Proust-Lima, Karen Leffondré","doi":"10.1186/s12940-024-01106-x","DOIUrl":"10.1186/s12940-024-01106-x","url":null,"abstract":"<p><strong>Background: </strong>While genetic, hormonal, and lifestyle factors partially elucidate the incidence of breast cancer, emerging research has underscored the potential contribution of air pollution. Polychlorinated biphenyls (PCBs) and benzo[a]pyrene (BaP) are of particular concern due to endocrine-disrupting properties and their carcinogenetic effect.</p><p><strong>Objective: </strong>To identify distinct long term trajectories of exposure to PCB153 and BaP, and estimate their associations with breast cancer risk.</p><p><strong>Methods: </strong>We used data from the XENAIR case-control study, nested within the ongoing prospective French E3N cohort which enrolled 98,995 women aged 40-65 years in 1990-1991. Cases were incident cases of primary invasive breast cancer diagnosed from cohort entry to 2011. Controls were randomly selected by incidence density sampling, and individually matched to cases on delay since cohort entry, and date, age, department of residence, and menopausal status at cohort entry. Annual mean outdoor PCB153 and BaP concentrations at residential addresses from 1990 to 2011 were estimated using the CHIMERE chemistry-transport model. Latent class mixed models were used to identify profiles of exposure trajectories from cohort entry to the index date, and conditional logistic regression to estimate their association with the odds of breast cancer.</p><p><strong>Results: </strong>5058 cases and 5059 controls contributed to the analysis. Five profiles of trajectories of PCB153 exposure were identified. The class with the highest PCB153 concentrations had a 69% increased odds of breast cancer compared to the class with the lowest concentrations (95% CI 1.08, 2.64), after adjustment for education and matching factors. The association between identified BaP trajectories and breast cancer was weaker and suffered from large CI.</p><p><strong>Conclusions: </strong>Our results support an association between long term exposure to PCB153 and the risk of breast cancer, and encourage further studies to account for lifetime exposure to persistent organic pollutants.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11380782/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142145406","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 : 2024-09-05DOI: 10.1186/s12940-023-01015-5
Shelley H Liu, Yitong Chen, David Bellinger, Erik de Water, Megan Horton, Martha M Téllez-Rojo, Robert Wright
Background: Neurodevelopmental performance tasks are often separately analyzed, even when they tap into a similar construct. This may yield mixed findings for associations of an exposure-neurobehavioral outcome. We develop an item response theory (IRT) approach to integrate multiple task variables together to improve measurement precision of the underlying construct. We apply this approach to create an integrative measure of childhood inhibitory control, and study impacts of pre/post-natal lead exposure.
Methods: Using data from a prospective cohort based in Mexico (N = 533), we created an inhibitory control scale that integrates accuracy and reaction time information from four inhibitory control tasks (Go/NoGo Letter, Go/NoGo Neutral, Go/NoGo Happy, Delis-Kaplan Executive Function System (D-KEFS) Color-Word Interference Test, Condition 3). Using a generalized partial credit item response theory model, we estimated an inhibitory control index for each participant. We then assessed adjusted associations between umbilical cord blood and 4-year lead and childhood inhibitory control. We developed a resampling approach to incorporate error estimates from the inhibitory control variable to confirm the consistency of the lead-inhibitory control associations. We modeled time-varying associations of lead with each inhibitory control measure separately.
Results: Participants had a median age of 9 years; 51.4% were males. Umbilical cord blood [-0.06 (95% CI: -0.11, -0.01)] and 4-year lead [-0.07 (95% CI: -0.12, -0.02)] were associated with inhibitory control index at 8-10 years. A resampling approach confirmed that 4-year lead was consistently associated with childhood inhibitory control index. Umbilical cord blood and 4-year lead were each associated with 3 out of 8 measures in separate models.
Conclusion: This is the first application of IRT in environmental epidemiology to create a latent variable for inhibitory control that integrates accuracy and reaction time information from multiple, related tasks. This framework can be applied to other correlated neurobehavioral assessments or other phenotype data.
{"title":"Pre-natal and early life lead exposure and childhood inhibitory control: an item response theory approach to improve measurement precision of inhibitory control.","authors":"Shelley H Liu, Yitong Chen, David Bellinger, Erik de Water, Megan Horton, Martha M Téllez-Rojo, Robert Wright","doi":"10.1186/s12940-023-01015-5","DOIUrl":"10.1186/s12940-023-01015-5","url":null,"abstract":"<p><strong>Background: </strong>Neurodevelopmental performance tasks are often separately analyzed, even when they tap into a similar construct. This may yield mixed findings for associations of an exposure-neurobehavioral outcome. We develop an item response theory (IRT) approach to integrate multiple task variables together to improve measurement precision of the underlying construct. We apply this approach to create an integrative measure of childhood inhibitory control, and study impacts of pre/post-natal lead exposure.</p><p><strong>Methods: </strong>Using data from a prospective cohort based in Mexico (N = 533), we created an inhibitory control scale that integrates accuracy and reaction time information from four inhibitory control tasks (Go/NoGo Letter, Go/NoGo Neutral, Go/NoGo Happy, Delis-Kaplan Executive Function System (D-KEFS) Color-Word Interference Test, Condition 3). Using a generalized partial credit item response theory model, we estimated an inhibitory control index for each participant. We then assessed adjusted associations between umbilical cord blood and 4-year lead and childhood inhibitory control. We developed a resampling approach to incorporate error estimates from the inhibitory control variable to confirm the consistency of the lead-inhibitory control associations. We modeled time-varying associations of lead with each inhibitory control measure separately.</p><p><strong>Results: </strong>Participants had a median age of 9 years; 51.4% were males. Umbilical cord blood [-0.06 (95% CI: -0.11, -0.01)] and 4-year lead [-0.07 (95% CI: -0.12, -0.02)] were associated with inhibitory control index at 8-10 years. A resampling approach confirmed that 4-year lead was consistently associated with childhood inhibitory control index. Umbilical cord blood and 4-year lead were each associated with 3 out of 8 measures in separate models.</p><p><strong>Conclusion: </strong>This is the first application of IRT in environmental epidemiology to create a latent variable for inhibitory control that integrates accuracy and reaction time information from multiple, related tasks. This framework can be applied to other correlated neurobehavioral assessments or other phenotype data.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11375946/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142132136","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 : 2024-09-04DOI: 10.1186/s12940-024-01110-1
Sara B A Mokhtar, Jessica Viljoen, Carla J H van der Kallen, Tos T J M Berendschot, Pieter C Dagnelie, Jeroen D Albers, Jens Soeterboek, Fabio Scarpa, Alessia Colonna, Frank C T van der Heide, Marleen M J van Greevenbroek, Hans Bosm, Abraham A Kroon, Rudy M M A Nuijts, Marlies Gijs, Jeroen Lakerveld, Rayaz A Malik, Carroll A B Webers, Coen D A Stehouwer, Annemarie Koster
Background: Epidemiological and toxicological studies indicate that increased exposure to air pollutants can lead to neurodegenerative diseases. To further confirm this relationship, we evaluated the association between exposure to ambient air pollutants and corneal nerve measures as a surrogate for neurodegeneration, using corneal confocal microscopy.
Methods: We used population-based observational cross-sectional data from The Maastricht Study including N = 3635 participants (mean age 59.3 years, 51.6% were women, and 19.9% had type 2 diabetes) living in the Maastricht area. Using the Geoscience and hEalth Cohort COnsortium (GECCO) data we linked the yearly average exposure levels of ambient air pollutants at home address-level [particulate matter with diameters of ≤ 2.5 µm (PM2.5), and ≤ 10.0 µm (PM10), nitrogen dioxide (NO2), and elemental carbon (EC)]. We used linear regression analysis to study the associations between Z-score for ambient air pollutants concentrations (PM2.5, PM10, NO2, and EC) and Z-score for individual corneal nerve measures (corneal nerve bifurcation density, corneal nerve density, corneal nerve length, and fractal dimension).
Results: After adjustment for potential confounders (age, sex, level of education, glucose metabolism status, corneal confocal microscopy lag time, inclusion year of participants, smoking status, and alcohol consumption), higher Z-scores for PM2.5 and PM10 were associated with lower Z-scores for corneal nerve bifurcation density, nerve density, nerve length, and nerve fractal dimension [stβ (95% CI): PM2.5 -0.10 (-0.14; -0.05), -0.04 (-0.09; 0.01), -0.11 (-0.16; -0.06), -0.20 (-0.24; -0.15); and PM10 -0.08 (-0.13; -0.03), -0.04 (-0.09; 0.01), -0.08 (-0.13; -0.04), -0.17 (-0.21; -0.12)], respectively. No associations were found between NO2 and EC and corneal nerve measures.
Conclusions: Our population-based study demonstrated that exposure to higher levels of PM2.5 and PM10 are associated with higher levels of corneal neurodegeneration, estimated from lower corneal nerve measures. Our results suggest that air pollution may be a determinant for neurodegeneration assessed in the cornea and may impact the ocular surface health as well.
{"title":"Greater exposure to PM<sub>2.5</sub> and PM<sub>10</sub> was associated with lower corneal nerve measures: the Maastricht study - a cross-sectional study.","authors":"Sara B A Mokhtar, Jessica Viljoen, Carla J H van der Kallen, Tos T J M Berendschot, Pieter C Dagnelie, Jeroen D Albers, Jens Soeterboek, Fabio Scarpa, Alessia Colonna, Frank C T van der Heide, Marleen M J van Greevenbroek, Hans Bosm, Abraham A Kroon, Rudy M M A Nuijts, Marlies Gijs, Jeroen Lakerveld, Rayaz A Malik, Carroll A B Webers, Coen D A Stehouwer, Annemarie Koster","doi":"10.1186/s12940-024-01110-1","DOIUrl":"10.1186/s12940-024-01110-1","url":null,"abstract":"<p><strong>Background: </strong>Epidemiological and toxicological studies indicate that increased exposure to air pollutants can lead to neurodegenerative diseases. To further confirm this relationship, we evaluated the association between exposure to ambient air pollutants and corneal nerve measures as a surrogate for neurodegeneration, using corneal confocal microscopy.</p><p><strong>Methods: </strong>We used population-based observational cross-sectional data from The Maastricht Study including N = 3635 participants (mean age 59.3 years, 51.6% were women, and 19.9% had type 2 diabetes) living in the Maastricht area. Using the Geoscience and hEalth Cohort COnsortium (GECCO) data we linked the yearly average exposure levels of ambient air pollutants at home address-level [particulate matter with diameters of ≤ 2.5 µm (PM2.5), and ≤ 10.0 µm (PM10), nitrogen dioxide (NO2), and elemental carbon (EC)]. We used linear regression analysis to study the associations between Z-score for ambient air pollutants concentrations (PM<sub>2.5</sub>, PM<sub>10</sub>, NO<sub>2</sub>, and EC) and Z-score for individual corneal nerve measures (corneal nerve bifurcation density, corneal nerve density, corneal nerve length, and fractal dimension).</p><p><strong>Results: </strong>After adjustment for potential confounders (age, sex, level of education, glucose metabolism status, corneal confocal microscopy lag time, inclusion year of participants, smoking status, and alcohol consumption), higher Z-scores for PM<sub>2.5</sub> and PM<sub>10</sub> were associated with lower Z-scores for corneal nerve bifurcation density, nerve density, nerve length, and nerve fractal dimension [stβ (95% CI): PM<sub>2.5</sub> -0.10 (-0.14; -0.05), -0.04 (-0.09; 0.01), -0.11 (-0.16; -0.06), -0.20 (-0.24; -0.15); and PM<sub>10</sub> -0.08 (-0.13; -0.03), -0.04 (-0.09; 0.01), -0.08 (-0.13; -0.04), -0.17 (-0.21; -0.12)], respectively. No associations were found between NO<sub>2</sub> and EC and corneal nerve measures.</p><p><strong>Conclusions: </strong>Our population-based study demonstrated that exposure to higher levels of PM<sub>2.5</sub> and PM<sub>10</sub> are associated with higher levels of corneal neurodegeneration, estimated from lower corneal nerve measures. Our results suggest that air pollution may be a determinant for neurodegeneration assessed in the cornea and may impact the ocular surface health as well.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11375839/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142132135","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 : 2024-08-30DOI: 10.1186/s12940-024-01109-8
Janice M Y Hu, Tye E Arbuckle, Patricia A Janssen, Bruce P Lanphear, Joshua D Alampi, Joseph M Braun, Amanda J MacFarlane, Aimin Chen, Lawrence C McCandless
{"title":"Correction: Gestational exposure to organochlorine compounds and metals and infant birth weight: effect modification by maternal hardships.","authors":"Janice M Y Hu, Tye E Arbuckle, Patricia A Janssen, Bruce P Lanphear, Joshua D Alampi, Joseph M Braun, Amanda J MacFarlane, Aimin Chen, Lawrence C McCandless","doi":"10.1186/s12940-024-01109-8","DOIUrl":"https://doi.org/10.1186/s12940-024-01109-8","url":null,"abstract":"","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11363617/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142105431","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 : 2024-08-13DOI: 10.1186/s12940-024-01107-w
Qi Meng, Sanjali Mitra, Irish Del Rosario, Michael Jerrett, Carla Janzen, Sherin U Devaskar, Beate Ritz
Background: Polycyclic aromatic hydrocarbons (PAHs) have been linked to adverse birth outcomes that have been reported to be induced by oxidative stress, but few epidemiological studies to date have evaluated associations between urinary PAH metabolites and oxidative stress biomarkers in pregnancy and identified critical periods for these outcomes and PAH exposures in pregnancy.
Methods: A cohort of pregnant women was recruited early in pregnancy from antenatal clinics at the University of California Los Angeles during 2016-2019. We collected urine samples up to three times during pregnancy in a total of 159 women enrolled in the cohort. A total of 7 PAH metabolites and 2 oxidative stress biomarkers [malondialdehyde (MDA), 8-hydroxy-2'-deoxyguanosine (8-OHdG)] were measured in all available urine samples. Using multiple linear regression models, we estimated the percentage change (%) and 95% confidence interval (CI) in 8-OHdG and MDA measured at each sample collection time per doubling of PAH metabolite concentrations. Furthermore, we used linear mixed models with a random intercept for participant to estimate the associations between PAH metabolite and oxidative stress biomarker concentrations across multiple time points in pregnancy.
Results: Most PAH metabolites were positively associated with both urinary oxidative stress biomarkers, MDA and 8-OHdG, with stronger associations in early and late pregnancy. A doubling of each urinary PAH metabolite concentration increased MDA concentrations by 5.8-41.1% and 8-OHdG concentrations by 13.8-49.7%. Linear mixed model results were consistent with those from linear regression models for each gestational sampling period.
Conclusion: Urinary PAH metabolites are associated with increases in oxidative stress biomarkers during pregnancy, especially in early and late pregnancy.
{"title":"Urinary polycyclic aromatic hydrocarbon metabolites and their association with oxidative stress among pregnant women in Los Angeles.","authors":"Qi Meng, Sanjali Mitra, Irish Del Rosario, Michael Jerrett, Carla Janzen, Sherin U Devaskar, Beate Ritz","doi":"10.1186/s12940-024-01107-w","DOIUrl":"10.1186/s12940-024-01107-w","url":null,"abstract":"<p><strong>Background: </strong>Polycyclic aromatic hydrocarbons (PAHs) have been linked to adverse birth outcomes that have been reported to be induced by oxidative stress, but few epidemiological studies to date have evaluated associations between urinary PAH metabolites and oxidative stress biomarkers in pregnancy and identified critical periods for these outcomes and PAH exposures in pregnancy.</p><p><strong>Methods: </strong>A cohort of pregnant women was recruited early in pregnancy from antenatal clinics at the University of California Los Angeles during 2016-2019. We collected urine samples up to three times during pregnancy in a total of 159 women enrolled in the cohort. A total of 7 PAH metabolites and 2 oxidative stress biomarkers [malondialdehyde (MDA), 8-hydroxy-2'-deoxyguanosine (8-OHdG)] were measured in all available urine samples. Using multiple linear regression models, we estimated the percentage change (%) and 95% confidence interval (CI) in 8-OHdG and MDA measured at each sample collection time per doubling of PAH metabolite concentrations. Furthermore, we used linear mixed models with a random intercept for participant to estimate the associations between PAH metabolite and oxidative stress biomarker concentrations across multiple time points in pregnancy.</p><p><strong>Results: </strong>Most PAH metabolites were positively associated with both urinary oxidative stress biomarkers, MDA and 8-OHdG, with stronger associations in early and late pregnancy. A doubling of each urinary PAH metabolite concentration increased MDA concentrations by 5.8-41.1% and 8-OHdG concentrations by 13.8-49.7%. Linear mixed model results were consistent with those from linear regression models for each gestational sampling period.</p><p><strong>Conclusion: </strong>Urinary PAH metabolites are associated with increases in oxidative stress biomarkers during pregnancy, especially in early and late pregnancy.</p>","PeriodicalId":11686,"journal":{"name":"Environmental Health","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11321171/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141975354","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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