Pub Date : 2022-08-31eCollection Date: 2022-10-01DOI: 10.1097/EE9.0000000000000222
Yu Zhang, Vicente Mustieles, Paige L Williams, Irene Souter, Antonia M Calafat, Melina Demokritou, Alexandria Lee, Stylianos Vagios, Russ Hauser, Carmen Messerlian
Although parental preconception exposure to some phenols and phthalates have been associated with reduced birthweight, few studies have examined these chemicals as complex mixtures.
Methods: We included 384 mothers and 211 fathers (203 couples) who gave birth to 384 singletons from a prospective cohort of couples seeking fertility evaluation. Urinary concentrations of bisphenol A (BPA), parabens, and 11 phthalate metabolites including those of di(2-ethylhexyl) phthalate (DEHP) were examined. Birthweight was abstracted from delivery records. We used principal component analysis and Bayesian Kernel Machine Regression (BKMR) to examine maternal and paternal preconception mixtures in relation to singleton birthweight. We also fit couple-based BKMR with hierarchical variable selection to assess couples' joint mixtures in relation to birthweight.
Results: PC scores of maternal and paternal preconception low molecular weight phthalates factor, and paternal preconception DEHP-BPA factor were associated with reduced birthweight. In BKMR models, we found that maternal preconception monoethyl phthalate and BPA concentrations, and paternal preconception mono-n-butyl phthalate concentrations were inversely associated with birthweight when the remaining mixture components were held at their median concentrations. In couple-based BKMR models, paternal preconception biomarkers contributed more to couples' joint effect on birthweight compared with maternal preconception biomarkers. A decreasing trend of birthweight was observed across quantiles of maternal, paternal, and couples' total preconception mixture concentrations, respectively.
Conclusions: Results from this preconception cohort of subfertile couples suggest a complex interplay between paternal and maternal preconception exposure to mixtures of nonpersistent chemicals, with both parental windows of exposure jointly contributing to reduced birthweight.
{"title":"Association of preconception mixtures of phenol and phthalate metabolites with birthweight among subfertile couples.","authors":"Yu Zhang, Vicente Mustieles, Paige L Williams, Irene Souter, Antonia M Calafat, Melina Demokritou, Alexandria Lee, Stylianos Vagios, Russ Hauser, Carmen Messerlian","doi":"10.1097/EE9.0000000000000222","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000222","url":null,"abstract":"<p><p>Although parental preconception exposure to some phenols and phthalates have been associated with reduced birthweight, few studies have examined these chemicals as complex mixtures.</p><p><strong>Methods: </strong>We included 384 mothers and 211 fathers (203 couples) who gave birth to 384 singletons from a prospective cohort of couples seeking fertility evaluation. Urinary concentrations of bisphenol A (BPA), parabens, and 11 phthalate metabolites including those of di(2-ethylhexyl) phthalate (DEHP) were examined. Birthweight was abstracted from delivery records. We used principal component analysis and Bayesian Kernel Machine Regression (BKMR) to examine maternal and paternal preconception mixtures in relation to singleton birthweight. We also fit couple-based BKMR with hierarchical variable selection to assess couples' joint mixtures in relation to birthweight.</p><p><strong>Results: </strong>PC scores of maternal and paternal preconception low molecular weight phthalates factor, and paternal preconception DEHP-BPA factor were associated with reduced birthweight. In BKMR models, we found that maternal preconception monoethyl phthalate and BPA concentrations, and paternal preconception mono-n-butyl phthalate concentrations were inversely associated with birthweight when the remaining mixture components were held at their median concentrations. In couple-based BKMR models, paternal preconception biomarkers contributed more to couples' joint effect on birthweight compared with maternal preconception biomarkers. A decreasing trend of birthweight was observed across quantiles of maternal, paternal, and couples' total preconception mixture concentrations, respectively.</p><p><strong>Conclusions: </strong>Results from this preconception cohort of subfertile couples suggest a complex interplay between paternal and maternal preconception exposure to mixtures of nonpersistent chemicals, with both parental windows of exposure jointly contributing to reduced birthweight.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2022-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9555928/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33516649","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-08-23eCollection Date: 2022-10-01DOI: 10.1097/EE9.0000000000000223
Vanessa R Coffman, Anja Søndergaard Jensen, Betina B Trabjerg, Carsten Bøcker Pedersen, Birgitte Hansen, Torben Sigsgaard, Jørn Olsen, Jörg Schullehner, Marie Pedersen, Leslie T Stayner
Evidence is emerging that preterm birth (PTB, birth before 37 completed weeks of gestation), a risk factor for neonatal mortality and future morbidity, may be induced by maternal nitrate ( ) exposure from drinking water. The objective of this study is to assess the association between maternal exposure to nitrate and the risk of PTB in a nationwide study of liveborn singletons.
Methods: We estimated maternal nitrate exposure from household tap water for 1,055,584 births in Denmark to Danish-born parents during 1991-2015 by linkage of individual home address(es) with nitrate concentrations from a national monitoring database. Nitrate exposure during pregnancy was modeled using four categories and continuously. Logistic models adjusted for sex, birth year, birth order, urbanicity, and maternal age, smoking, education, income, and employment, with generalized estimating equations were used to account for sibling clusters.
Results: A total of 1,009,189 births were included, comprising 51,747 PTB. An increase in the risk of PTB was seen across categories of exposure (P < 0.001) with an odds ratio (OR) in the uppermost category (>25 mg/L nitrate) of 1.05 (95% confidence interval [CI] = 1.00, 1.10). Evidence of an exposure-response relationship was observed in models using continuous nitrate (OR = 1.01 [95% CI = 1.00, 1.03] per 10 mg/L nitrate). In sensitivity analyses, results were robust to the addition of variables for short inter-pregnancy interval (<1 year between births), maternal pre-pregnancy body mass index, paternal socioeconomic status and age, season of birth, and inclusion of post-term births. Results were virtually unchanged when the analysis was restricted to women exposed to less than the current European Union standard of 50 mg/L.
Conclusion: We observed an increasing risk of PTB with increases in nitrate in household tap water. These findings add to a growing body of evidence of adverse effects from nitrate in drinking water at levels below current regulatory levels.
{"title":"Prenatal exposure to nitrate from drinking water and the risk of preterm birth: A Danish nationwide cohort study.","authors":"Vanessa R Coffman, Anja Søndergaard Jensen, Betina B Trabjerg, Carsten Bøcker Pedersen, Birgitte Hansen, Torben Sigsgaard, Jørn Olsen, Jörg Schullehner, Marie Pedersen, Leslie T Stayner","doi":"10.1097/EE9.0000000000000223","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000223","url":null,"abstract":"<p><p>Evidence is emerging that preterm birth (PTB, birth before 37 completed weeks of gestation), a risk factor for neonatal mortality and future morbidity, may be induced by maternal nitrate ( <math> <mstyle> <msubsup><mrow><mi>N</mi> <mi>O</mi></mrow> <mrow><mn>3</mn></mrow> <mrow><mo>-</mo></mrow> </msubsup> </mstyle> </math> ) exposure from drinking water. The objective of this study is to assess the association between maternal exposure to nitrate and the risk of PTB in a nationwide study of liveborn singletons.</p><p><strong>Methods: </strong>We estimated maternal nitrate exposure from household tap water for 1,055,584 births in Denmark to Danish-born parents during 1991-2015 by linkage of individual home address(es) with nitrate concentrations from a national monitoring database. Nitrate exposure during pregnancy was modeled using four categories and continuously. Logistic models adjusted for sex, birth year, birth order, urbanicity, and maternal age, smoking, education, income, and employment, with generalized estimating equations were used to account for sibling clusters.</p><p><strong>Results: </strong>A total of 1,009,189 births were included, comprising 51,747 PTB. An increase in the risk of PTB was seen across categories of exposure (<i>P</i> < 0.001) with an odds ratio (OR) in the uppermost category (>25 mg/L nitrate) of 1.05 (95% confidence interval [CI] = 1.00, 1.10). Evidence of an exposure-response relationship was observed in models using continuous nitrate (OR = 1.01 [95% CI = 1.00, 1.03] per 10 mg/L nitrate). In sensitivity analyses, results were robust to the addition of variables for short inter-pregnancy interval (<1 year between births), maternal pre-pregnancy body mass index, paternal socioeconomic status and age, season of birth, and inclusion of post-term births. Results were virtually unchanged when the analysis was restricted to women exposed to less than the current European Union standard of 50 mg/L.</p><p><strong>Conclusion: </strong>We observed an increasing risk of PTB with increases in nitrate in household tap water. These findings add to a growing body of evidence of adverse effects from nitrate in drinking water at levels below current regulatory levels.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2022-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/f3/cc/ee9-6-e223.PMC9556052.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33516648","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-08-15eCollection Date: 2022-10-01DOI: 10.1097/EE9.0000000000000224
Stephanie M Eick, Lara Cushing, Dana E Goin, Amy M Padula, Aileen Andrade, Erin DeMicco, Tracey J Woodruff, Rachel Morello-Frosch
Living in a disadvantaged neighborhood has been associated with adverse birth outcomes. Most prior studies have conceptualized neighborhoods using census boundaries and few have examined the role of neighborhood perceptions, which may better capture the neighborhood environment. In the present study, we examined associations between extrinsic and perceived neighborhood quality measures and adverse birth outcomes.
Methods: Participants resided in the San Francisco Bay Area of California and were enrolled in Chemicals in Our Bodies, a prospective birth cohort (N = 817). The Index of Concentration at the Extremes (ICE) for income, Area Deprivation Index (ADI), and the Urban Displacement Project's measure of gentrification were included as census block group-level extrinsic neighborhood quality measures. Poor perceived neighborhood quality was assessed using an interview questionnaire. Linear regression models were utilized to examine associations between extrinsic and perceived neighborhood quality measures, and gestational age and birthweight for gestational age z-scores. Covariates in adjusted models were chosen via a directed acyclic graph (DAG) and included maternal age, education, and marital status.
Results: In adjusted models, having poor perceived neighborhood quality was associated with higher birthweight z-scores, relative to those who did not perceive their neighborhood as poor quality (β = 0.21, 95% confidence intervals = 0.01, 0.42). Relative to the least disadvantaged tertile, the upper tertile of the ADI was associated with a modest reduction in gestational age (β = -0.35, 95% confidence intervals = -0.67, -0.02).
Conclusions: In the Chemicals in Our Bodies study population, extrinsic and perceived neighborhood quality measures were inconsistently associated with adverse birth outcomes.
{"title":"Neighborhood conditions and birth outcomes: Understanding the role of perceived and extrinsic measures of neighborhood quality.","authors":"Stephanie M Eick, Lara Cushing, Dana E Goin, Amy M Padula, Aileen Andrade, Erin DeMicco, Tracey J Woodruff, Rachel Morello-Frosch","doi":"10.1097/EE9.0000000000000224","DOIUrl":"10.1097/EE9.0000000000000224","url":null,"abstract":"<p><p>Living in a disadvantaged neighborhood has been associated with adverse birth outcomes. Most prior studies have conceptualized neighborhoods using census boundaries and few have examined the role of neighborhood perceptions, which may better capture the neighborhood environment. In the present study, we examined associations between extrinsic and perceived neighborhood quality measures and adverse birth outcomes.</p><p><strong>Methods: </strong>Participants resided in the San Francisco Bay Area of California and were enrolled in Chemicals in Our Bodies, a prospective birth cohort (N = 817). The Index of Concentration at the Extremes (ICE) for income, Area Deprivation Index (ADI), and the Urban Displacement Project's measure of gentrification were included as census block group-level extrinsic neighborhood quality measures. Poor perceived neighborhood quality was assessed using an interview questionnaire. Linear regression models were utilized to examine associations between extrinsic and perceived neighborhood quality measures, and gestational age and birthweight for gestational age z-scores. Covariates in adjusted models were chosen via a directed acyclic graph (DAG) and included maternal age, education, and marital status.</p><p><strong>Results: </strong>In adjusted models, having poor perceived neighborhood quality was associated with higher birthweight z-scores, relative to those who did not perceive their neighborhood as poor quality (β = 0.21, 95% confidence intervals = 0.01, 0.42). Relative to the least disadvantaged tertile, the upper tertile of the ADI was associated with a modest reduction in gestational age (β = -0.35, 95% confidence intervals = -0.67, -0.02).</p><p><strong>Conclusions: </strong>In the Chemicals in Our Bodies study population, extrinsic and perceived neighborhood quality measures were inconsistently associated with adverse birth outcomes.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2022-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9555921/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9939548","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-08-01DOI: 10.1097/EE9.0000000000000216
Lyndsey K Blair, Erica T Warner, Peter James, Jaime E Hart, Trang VoPham, Mollie E Barnard, Johnnie D Newton, Divya J Murthy, Francine Laden, Rulla M Tamimi, Natalie C DuPre
Inverse associations between natural vegetation exposure (i.e., greenness) and breast cancer risk have been reported; however, it remains unknown whether greenness affects breast tissue development or operates through other mechanisms (e.g., body mass index [BMI] or physical activity). We examined the association between greenness and mammographic density-a strong breast cancer risk factor-to determine whether greenness influences breast tissue composition independent of lifestyle factors.
Methods: Women (n = 2,318) without a history of breast cancer underwent mammographic screening at Brigham and Women's Hospital in Boston, Massachusetts, from 2006 to 2014. Normalized Difference Vegetation Index (NDVI) satellite data at 1-km2 resolution were used to estimate greenness at participants' residential address 1, 3, and 5 years before mammogram. We used multivariable linear regression to estimate differences in log-transformed volumetric mammographic density measures and 95% confidence intervals (CIs) for each 0.1 unit increase in NDVI.
Results: Five-year annual average NDVI was not associated with percent mammographic density in premenopausal (β = -0.01; 95% CI = -0.03, 0.02; P = 0.58) and postmenopausal women (β = -0.02; 95% CI = -0.04, 0.01; P = 0.18). Results were similar for 1-year and 3-year NDVI measures and in models including potential mediators of BMI and physical activity. There were also no associations between greenness and dense volume and nondense volume.
Conclusions: Greenness exposures were not associated with mammographic density.
Impact: Prior observations of a protective association between greenness and breast cancer may not be driven by differences in breast tissue composition, as measured by mammographic density, but rather other mechanisms.
据报道,自然植被暴露(即绿色)与乳腺癌风险呈负相关;然而,尚不清楚绿色是否会影响乳房组织发育或通过其他机制(例如,体重指数[BMI]或身体活动)起作用。我们研究了绿度和乳房x线摄影密度之间的关系——一个强有力的乳腺癌风险因素——以确定绿度是否独立于生活方式因素影响乳房组织组成。方法:2006年至2014年,无乳腺癌病史的女性(n = 2318)在马萨诸塞州波士顿布里格姆妇女医院接受了乳房x光检查。使用1平方公里分辨率的归一化植被指数(NDVI)卫星数据来估计参与者在乳房x光检查前1、3和5年的居住地址的绿化率。我们使用多变量线性回归来估计对数转换的乳腺容积密度测量值和NDVI每增加0.1个单位的95%置信区间(ci)的差异。结果:绝经前患者5年平均NDVI与乳腺x线摄影密度百分比无关(β = -0.01;95% ci = -0.03, 0.02;P = 0.58)和绝经后妇女(β = -0.02;95% ci = -0.04, 0.01;P = 0.18)。1年和3年NDVI测量以及包括BMI和身体活动的潜在介质的模型的结果相似。绿化率与密集体积和非密集体积之间也没有关联。结论:绿色暴露与乳腺x线摄影密度无关。影响:先前观察到的绿色与乳腺癌之间的保护性关联可能不是由乳房组织组成的差异驱动的,由乳房x线摄影密度测量,而是其他机制。
{"title":"Exposure to natural vegetation in relation to mammographic density in a Massachusetts-based clinical cohort.","authors":"Lyndsey K Blair, Erica T Warner, Peter James, Jaime E Hart, Trang VoPham, Mollie E Barnard, Johnnie D Newton, Divya J Murthy, Francine Laden, Rulla M Tamimi, Natalie C DuPre","doi":"10.1097/EE9.0000000000000216","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000216","url":null,"abstract":"<p><p>Inverse associations between natural vegetation exposure (i.e., greenness) and breast cancer risk have been reported; however, it remains unknown whether greenness affects breast tissue development or operates through other mechanisms (e.g., body mass index [BMI] or physical activity). We examined the association between greenness and mammographic density-a strong breast cancer risk factor-to determine whether greenness influences breast tissue composition independent of lifestyle factors.</p><p><strong>Methods: </strong>Women (n = 2,318) without a history of breast cancer underwent mammographic screening at Brigham and Women's Hospital in Boston, Massachusetts, from 2006 to 2014. Normalized Difference Vegetation Index (NDVI) satellite data at 1-km<sup>2</sup> resolution were used to estimate greenness at participants' residential address 1, 3, and 5 years before mammogram. We used multivariable linear regression to estimate differences in log-transformed volumetric mammographic density measures and 95% confidence intervals (CIs) for each 0.1 unit increase in NDVI.</p><p><strong>Results: </strong>Five-year annual average NDVI was not associated with percent mammographic density in premenopausal (β = -0.01; 95% CI = -0.03, 0.02; <i>P</i> = 0.58) and postmenopausal women (β = -0.02; 95% CI = -0.04, 0.01; <i>P</i> = 0.18). Results were similar for 1-year and 3-year NDVI measures and in models including potential mediators of BMI and physical activity. There were also no associations between greenness and dense volume and nondense volume.</p><p><strong>Conclusions: </strong>Greenness exposures were not associated with mammographic density.</p><p><strong>Impact: </strong>Prior observations of a protective association between greenness and breast cancer may not be driven by differences in breast tissue composition, as measured by mammographic density, but rather other mechanisms.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/34/94/ee9-6-e216.PMC9374192.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9777960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-08-01DOI: 10.1097/EE9.0000000000000214
Christine Kim, Amber L Cathey, Deborah J Watkins, Bhramar Mukherjee, Zaira Y Rosario-Pabón, Carmen M Vélez-Vega, Akram N Alshawabkeh, José F Cordero, John D Meeker
Studies have revealed a link between aberrant levels of maternal C-reactive protein (CRP) and cell adhesion molecules (CAMs) with adverse birth outcomes. Some epidemiologic studies have indicated that long-term metal exposures can modulate the levels of CRP and CAMs, but the associations between prenatal metal exposures and the levels of CRP and CAMs have yet to be studied more extensively. In this study, we assessed associations between maternal blood metal levels and CRP/CAMs among 617 pregnant women in the Puerto Rico PROTECT birth cohort.
Methods: Blood samples were collected from participants at 16-20 (visit 1) and 24-28 (visit 3) weeks gestation. We measured concentrations of 11 metals using inductively coupled plasma mass spectrometry (ICP-MS). From the blood samples, CRP and CAMs intercellular adhesion molecule (ICAM) and vascular cell adhesion molecule (VCAM) were also quantified using a customized Luminex assay. Linear-mixed effects models (LMEs) were used to regress CRP and CAMs on metals and included random intercepts for study participants to account for correlated repeated outcome measures. Fetal sex and visit effects were estimated using interaction terms between metal exposure variables and fetal sex, as well as visit indicators, respectively.
Results: We observed significant positive associations between nickel and CRP (Δ: 7.04, 95% CI = 0.75, 13.73) and between lead and VCAM (Δ: 4.57, 95% CI = 1.36, 7.89). The positive associations were mainly driven by mothers carrying male fetuses. We also observed various visit-specific associations. The significant associations between metals and CRP were predominantly driven by visit 3; however, the significant associations between metals and VCAM were mainly driven by visit 1.
Conclusion: Certain maternal blood metal levels were significantly associated with CRP and CAMs and most of these associations were differentially driven by fetal sex, as well as by timing in pregnancy. Future studies should further explore metal-CRP/CAMs associations for a better understanding of the underlying mechanism of metal-induced adverse birth outcomes.
研究揭示了母体c反应蛋白(CRP)和细胞粘附分子(CAMs)异常水平与不良出生结局之间的联系。一些流行病学研究表明,长期金属暴露可以调节CRP和CAMs的水平,但产前金属暴露与CRP和CAMs水平之间的关系尚未得到更广泛的研究。在这项研究中,我们评估了波多黎各PROTECT出生队列中617名孕妇的母亲血金属水平与CRP/ cam之间的关系。方法:在妊娠16-20周(第1次访问)和24-28周(第3次访问)采集血样。我们用电感耦合等离子体质谱(ICP-MS)测量了11种金属的浓度。从血液样本中,CRP和cam细胞间粘附分子(ICAM)和血管细胞粘附分子(VCAM)也使用定制的Luminex测定法进行定量。线性混合效应模型(LMEs)用于回归CRP和金属上的cam,并包括研究参与者的随机截点,以解释相关的重复结果测量。利用金属暴露变量和胎儿性别之间的相互作用项,以及访问指标,分别估计胎儿性别和访问效应。结果:我们观察到镍和CRP (Δ: 7.04, 95% CI = 0.75, 13.73)以及铅和VCAM (Δ: 4.57, 95% CI = 1.36, 7.89)之间存在显著的正相关。这种积极的联系主要是由携带男性胎儿的母亲推动的。我们还观察到不同的访问特异性关联。金属和CRP之间的显著关联主要是由第3次访问驱动的;然而,金属与VCAM之间的显著关联主要是由访问1驱动的。结论:某些母体血金属水平与CRP和CAMs有显著相关性,且这些相关性主要受胎儿性别和妊娠时间的影响。未来的研究应进一步探索金属- crp /CAMs的关联,以更好地了解金属诱导不良出生结局的潜在机制。
{"title":"Maternal blood metal concentrations are associated with C-reactive protein and cell adhesion molecules among pregnant women in Puerto Rico.","authors":"Christine Kim, Amber L Cathey, Deborah J Watkins, Bhramar Mukherjee, Zaira Y Rosario-Pabón, Carmen M Vélez-Vega, Akram N Alshawabkeh, José F Cordero, John D Meeker","doi":"10.1097/EE9.0000000000000214","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000214","url":null,"abstract":"<p><p>Studies have revealed a link between aberrant levels of maternal C-reactive protein (CRP) and cell adhesion molecules (CAMs) with adverse birth outcomes. Some epidemiologic studies have indicated that long-term metal exposures can modulate the levels of CRP and CAMs, but the associations between prenatal metal exposures and the levels of CRP and CAMs have yet to be studied more extensively. In this study, we assessed associations between maternal blood metal levels and CRP/CAMs among 617 pregnant women in the Puerto Rico PROTECT birth cohort.</p><p><strong>Methods: </strong>Blood samples were collected from participants at 16-20 (visit 1) and 24-28 (visit 3) weeks gestation. We measured concentrations of 11 metals using inductively coupled plasma mass spectrometry (ICP-MS). From the blood samples, CRP and CAMs intercellular adhesion molecule (ICAM) and vascular cell adhesion molecule (VCAM) were also quantified using a customized Luminex assay. Linear-mixed effects models (LMEs) were used to regress CRP and CAMs on metals and included random intercepts for study participants to account for correlated repeated outcome measures. Fetal sex and visit effects were estimated using interaction terms between metal exposure variables and fetal sex, as well as visit indicators, respectively.</p><p><strong>Results: </strong>We observed significant positive associations between nickel and CRP (Δ: 7.04, 95% CI = 0.75, 13.73) and between lead and VCAM (Δ: 4.57, 95% CI = 1.36, 7.89). The positive associations were mainly driven by mothers carrying male fetuses. We also observed various visit-specific associations. The significant associations between metals and CRP were predominantly driven by visit 3; however, the significant associations between metals and VCAM were mainly driven by visit 1.</p><p><strong>Conclusion: </strong>Certain maternal blood metal levels were significantly associated with CRP and CAMs and most of these associations were differentially driven by fetal sex, as well as by timing in pregnancy. Future studies should further explore metal-CRP/CAMs associations for a better understanding of the underlying mechanism of metal-induced adverse birth outcomes.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9374188/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10351725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-08-01DOI: 10.1097/EE9.0000000000000217
Cavin K Ward-Caviness, Joshua Moyer, Anne Weaver, Robert Devlin, David Diaz-Sanchez
Per and polyfluoroalkyl substances (PFAS) are associated with health outcomes ranging from cancer to high cholesterol. However, there has been little examination of how PFAS exposure might impact the development of multiple chronic diseases, known as multimorbidity. Here, we associated the presence of one or more PFAS in water systems serving the zip code of residence with chronic disease and multimorbidity.
Methods: We used data from the unregulated contaminant monitoring rule 3 to estimate exposure to PFAS for a random sample of 10,168 patients from the University of North Carolina Healthcare System. The presence of 16 chronic diseases was determined via. their electronic health records. We used a logistic regression model in a cross-sectional study design to associate the presence of one or more PFAS with multimorbidity. Models were adjusted for age, race, sex, smoking status, socioeconomic status, and 20 county-level confounders.
Results: There were four PFAS found in water systems that served at least one zip code represented in our patient data: PFOA, PFHpA, PFOS, and PFHxS. Exposure to any PFAS was associated with a odds ratio of 1.25 for multimorbidity (95% confidence interval = 1.09, 1.45). Among the chronic diseases with at least 300 cases, we observed associations with dyslipidemia, hypertension, ischemic heart disease, and osteoporosis.
Conclusion: Exposure to PFAS is associated with a range of chronic diseases as well as multimorbidity. Accounting for the joint impacts of PFAS on multiple chronic conditions may give an increasingly clear picture of the public health impacts of PFAS.
{"title":"Associations between PFAS occurrence and multimorbidity as observed in an electronic health record cohort.","authors":"Cavin K Ward-Caviness, Joshua Moyer, Anne Weaver, Robert Devlin, David Diaz-Sanchez","doi":"10.1097/EE9.0000000000000217","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000217","url":null,"abstract":"<p><p>Per and polyfluoroalkyl substances (PFAS) are associated with health outcomes ranging from cancer to high cholesterol. However, there has been little examination of how PFAS exposure might impact the development of multiple chronic diseases, known as multimorbidity. Here, we associated the presence of one or more PFAS in water systems serving the zip code of residence with chronic disease and multimorbidity.</p><p><strong>Methods: </strong>We used data from the unregulated contaminant monitoring rule 3 to estimate exposure to PFAS for a random sample of 10,168 patients from the University of North Carolina Healthcare System. The presence of 16 chronic diseases was determined via. their electronic health records. We used a logistic regression model in a cross-sectional study design to associate the presence of one or more PFAS with multimorbidity. Models were adjusted for age, race, sex, smoking status, socioeconomic status, and 20 county-level confounders.</p><p><strong>Results: </strong>There were four PFAS found in water systems that served at least one zip code represented in our patient data: PFOA, PFHpA, PFOS, and PFHxS. Exposure to any PFAS was associated with a odds ratio of 1.25 for multimorbidity (95% confidence interval = 1.09, 1.45). Among the chronic diseases with at least 300 cases, we observed associations with dyslipidemia, hypertension, ischemic heart disease, and osteoporosis.</p><p><strong>Conclusion: </strong>Exposure to PFAS is associated with a range of chronic diseases as well as multimorbidity. Accounting for the joint impacts of PFAS on multiple chronic conditions may give an increasingly clear picture of the public health impacts of PFAS.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9374186/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9756744","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-07-22eCollection Date: 2022-08-01DOI: 10.1097/EE9.0000000000000215
Marcus Dahlquist, Viveka Frykman, Massimo Stafoggia, Eva Qvarnström, Gregory A Wellenius, Petter L S Ljungman
Atrial fibrillation (AF) is the most common cardiac arrhythmia and is associated with substantial morbidity and mortality. Short-term exposure to fine particulate matter (PM2.5) has been causally linked to higher risk of cardiovascular disease, but the association with atrial fibrillation (AF) is less clear.
Methods: We conducted a time-stratified case-crossover study to estimate the association between short-term air pollution levels and risk of AF episodes. The episodes were identified among patients with paroxysmal AF and an intracardiac devices able to register and store AF episodes. We obtained air pollution and temperature data from fixed monitoring stations and used conditional logistic regression to quantify the association of PM2.5, particulate matter (PM10), nitrogen dioxide (NO2) and ozone (O3) with onset of AF episodes, adjusting for temperature and public holidays.".
Results: We analyzed 584 episodes of AF from 91 participants and observed increased risk of AF episodes with PM2.5 levels for the 48-72 hours lag (OR 1.05; CI [1.01,1.09] per IQR)] and 72-96 hours (OR 1.05 CI [1.00,1.10] per IQR). Our results were suggestive of an association between O3 levels and AF episodes during the warm season. We did not observe any statistically significant associations for PM10 nor NO2.
Conclusion: Short-term increases in PM2.5 in a low-pollution level environment were associated with increased risk of AF episodes in a population with intracardiac devices. Our findings add to the evidence of a potential triggering of AF by short-term increases in air pollution levels, well below the new WHO air quality guidelines.
心房颤动(AF)是最常见的心律失常,与大量的发病率和死亡率有关。短期暴露于细颗粒物(PM2.5)与较高的心血管疾病风险有因果关系,但与心房颤动(AF)的关系却不太清楚:我们进行了一项时间分层病例交叉研究,以估计短期空气污染水平与房颤发作风险之间的关系。房颤发作是从阵发性房颤患者和能够记录和存储房颤发作的心内设备中识别出来的。我们从固定监测站获得了空气污染和温度数据,并使用条件逻辑回归量化了 PM2.5、颗粒物(PM10)、二氧化氮(NO2)和臭氧(O3)与房颤发作的关联,同时对温度和公共假期进行了调整:我们对 91 名参与者的 584 次房颤发作进行了分析,观察到在 PM2.5 水平滞后 48-72 小时(OR 1.05;CI [1.01,1.09] per IQR)]和 72-96 小时(OR 1.05 CI [1.00,1.10] per IQR)时,房颤发作的风险增加。我们的研究结果表明,在温暖季节,臭氧水平与房颤发作之间存在关联。我们没有观察到 PM10 或 NO2.5 与心房颤动发作有任何统计学意义上的关联:结论:在一个低污染水平的环境中,PM2.5 的短期增加与使用心内装置的人群房颤发作风险的增加有关。我们的研究结果进一步证明,空气污染水平的短期升高可能会诱发房颤,而这一水平远低于世界卫生组织新的空气质量指南。
{"title":"Short-term ambient air pollution exposure and risk of atrial fibrillation in patients with intracardiac devices.","authors":"Marcus Dahlquist, Viveka Frykman, Massimo Stafoggia, Eva Qvarnström, Gregory A Wellenius, Petter L S Ljungman","doi":"10.1097/EE9.0000000000000215","DOIUrl":"10.1097/EE9.0000000000000215","url":null,"abstract":"<p><p>Atrial fibrillation (AF) is the most common cardiac arrhythmia and is associated with substantial morbidity and mortality. Short-term exposure to fine particulate matter (PM<sub>2.5</sub>) has been causally linked to higher risk of cardiovascular disease, but the association with atrial fibrillation (AF) is less clear.</p><p><strong>Methods: </strong>We conducted a time-stratified case-crossover study to estimate the association between short-term air pollution levels and risk of AF episodes. The episodes were identified among patients with paroxysmal AF and an intracardiac devices able to register and store AF episodes. We obtained air pollution and temperature data from fixed monitoring stations and used conditional logistic regression to quantify the association of PM<sub>2.5</sub>, particulate matter (PM<sub>10</sub>), nitrogen dioxide (NO<sub>2</sub>) and ozone (O<sub>3</sub>) with onset of AF episodes, adjusting for temperature and public holidays.\".</p><p><strong>Results: </strong>We analyzed 584 episodes of AF from 91 participants and observed increased risk of AF episodes with PM<sub>2.5</sub> levels for the 48-72 hours lag (OR 1.05; CI [1.01,1.09] per IQR)] and 72-96 hours (OR 1.05 CI [1.00,1.10] per IQR). Our results were suggestive of an association between O<sub>3</sub> levels and AF episodes during the warm season. We did not observe any statistically significant associations for PM<sub>10</sub> nor NO<sub>2</sub>.</p><p><strong>Conclusion: </strong>Short-term increases in PM<sub>2.5</sub> in a low-pollution level environment were associated with increased risk of AF episodes in a population with intracardiac devices. Our findings add to the evidence of a potential triggering of AF by short-term increases in air pollution levels, well below the new WHO air quality guidelines.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2022-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/f6/77/ee9-6-e215.PMC9374182.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40716195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-07-19eCollection Date: 2022-08-01DOI: 10.1097/EE9.0000000000000219
Leslie Michele-Ange Kouam Youogo, Marie-Elise Parent, Perry Hystad, Paul J Villeneuve
Ambient air pollution is a human carcinogen and a possible risk factor for prostate cancer.
Methods: We investigated associations between ambient concentrations particulate matter 2.5 (PM2.5) and nitrogen dioxide (NO2) and incident prostate cancer in a Canadian case-control study. Between 1994 and 1997, cases were identified from provincial cancer registries, and a population-based series of controls was recruited. Among men 50 years of age or older, risk factor and residential history data (1975 to 1994) were collected from 1,420 prostate cancer cases and 1,424 controls. Three methods were used to estimate the residential mean exposure to PM2.5 and NO2 during this period: (1) satellite-derived observations; (2) satellite-derived observations scaled with historical fixed-site measurements; and (3) a national land-use regression (LUR) model. Odds ratios (ORs) and their 95% confidence intervals (CIs) in relation to interquartile range (IQR) increases in PM2.5 and NO2 were estimated using logistic regression, adjusting for personal and contextual factors.
Results: We found positive associations between exposure to PM2.5 and NO2 over the previous 20 years and prostate cancer. An IQR increase in PM2.5 (3.56 µg/m3 for satellite and 4.48 µg/m3 for scaled satellite observations) yielded ORs of 1.28 (95% CI = 1.07, 1.52) and 1.20 (95% CI = 1.03, 1.40), respectively. For NO2, IQR increases (1.45 ppb for satellite, 15.18 ppb for scaled satellite-derived information, and 15.39 ppb for the national LUR) were associated with ORs of 1.09 (95% CI = 0.95, 1.24), 1.21 (95% CI = 1.02, 1.43), and 1.19 (95% CI = 1.03, 1.38), respectively.
Conclusions: Our findings support the hypothesis that ambient air pollution increases the risk of prostate cancer.
环境空气污染是一种人类致癌物,也是前列腺癌的可能危险因素。方法:我们在加拿大的一项病例对照研究中调查了环境颗粒物2.5 (PM2.5)和二氧化氮(NO2)浓度与前列腺癌发病率的关系。在1994年至1997年期间,从省级癌症登记处确定病例,并招募了基于人群的一系列对照。在50岁或以上的男性中,收集了1420例前列腺癌病例和1424例对照的风险因素和居住史数据(1975年至1994年)。利用3种方法估算了这一时期居民PM2.5和NO2的平均暴露量:(1)卫星观测;(2)基于历史固定地点测量的卫星观测数据;(3)国家土地利用回归(LUR)模型。在调整个人和环境因素后,使用逻辑回归估计PM2.5和NO2的比值比(ORs)及其与四分位数范围(IQR)增加相关的95%置信区间(ci)。结果:我们发现在过去20年中暴露于PM2.5和二氧化氮与前列腺癌之间存在正相关。PM2.5的IQR增加(卫星观测值为3.56µg/m3,缩放卫星观测值为4.48µg/m3)分别产生1.28 (95% CI = 1.07, 1.52)和1.20 (95% CI = 1.03, 1.40)。对于NO2, IQR增加(卫星1.45 ppb,卫星衍生信息15.18 ppb,国家LUR 15.39 ppb)的or分别为1.09 (95% CI = 0.95, 1.24), 1.21 (95% CI = 1.02, 1.43)和1.19 (95% CI = 1.03, 1.38)。结论:我们的研究结果支持了环境空气污染增加前列腺癌风险的假设。
{"title":"Ambient air pollution and prostate cancer risk in a population-based Canadian case-control study.","authors":"Leslie Michele-Ange Kouam Youogo, Marie-Elise Parent, Perry Hystad, Paul J Villeneuve","doi":"10.1097/EE9.0000000000000219","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000219","url":null,"abstract":"<p><p>Ambient air pollution is a human carcinogen and a possible risk factor for prostate cancer.</p><p><strong>Methods: </strong>We investigated associations between ambient concentrations particulate matter 2.5 (PM<sub>2.5</sub>) and nitrogen dioxide (NO<sub>2</sub>) and incident prostate cancer in a Canadian case-control study. Between 1994 and 1997, cases were identified from provincial cancer registries, and a population-based series of controls was recruited. Among men 50 years of age or older, risk factor and residential history data (1975 to 1994) were collected from 1,420 prostate cancer cases and 1,424 controls. Three methods were used to estimate the residential mean exposure to PM<sub>2.5</sub> and NO<sub>2</sub> during this period: (1) satellite-derived observations; (2) satellite-derived observations scaled with historical fixed-site measurements; and (3) a national land-use regression (LUR) model. Odds ratios (ORs) and their 95% confidence intervals (CIs) in relation to interquartile range (IQR) increases in PM<sub>2.5</sub> and NO<sub>2</sub> were estimated using logistic regression, adjusting for personal and contextual factors.</p><p><strong>Results: </strong>We found positive associations between exposure to PM<sub>2.5</sub> and NO<sub>2</sub> over the previous 20 years and prostate cancer. An IQR increase in PM<sub>2.5</sub> (3.56 µg/m<sup>3</sup> for satellite and 4.48 µg/m<sup>3</sup> for scaled satellite observations) yielded ORs of 1.28 (95% CI = 1.07, 1.52) and 1.20 (95% CI = 1.03, 1.40), respectively. For NO<sub>2</sub>, IQR increases (1.45 ppb for satellite, 15.18 ppb for scaled satellite-derived information, and 15.39 ppb for the national LUR) were associated with ORs of 1.09 (95% CI = 0.95, 1.24), 1.21 (95% CI = 1.02, 1.43), and 1.19 (95% CI = 1.03, 1.38), respectively.</p><p><strong>Conclusions: </strong>Our findings support the hypothesis that ambient air pollution increases the risk of prostate cancer.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2022-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9374191/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40633126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-06-29eCollection Date: 2022-08-01DOI: 10.1097/EE9.0000000000000218
Tara P McAlexander, Jyotsna S Jagai, Leslie A McClure
The prevalence of type 2 diabetes (T2D) has increased in the United States, and recent studies suggest that environmental factors contribute to T2D risk. We sought to understand if environmental factors were associated with the rate and magnitude of increase in diabetes prevalence at the county level.
Methods: We obtained age-adjusted diabetes prevalence estimates from the CDC for 3,137 US counties from 2004 to 2017. We applied latent growth mixture models to these data to identify classes of counties with similar trends in diabetes prevalence over time, stratified by Rural Urban Continuum Codes (RUCC). We then compared mean values of the US EPA Environmental Quality Index (EQI) 2006-2010, overall and for each of the five domain indices (air, water, land, sociodemographic, and built), with RUCC-specific latent class to examine associations of environmental factors and class of diabetes prevalence trajectory.
Results: Overall diabetes prevalence trends between 2004 and 2017 were similar across all RUCC strata. We identified two classes among metropolitan urbanized (RUCC 1) counties; four classes among non-metro urbanized (RUCC 2) counties; and three classes among less urbanized (RUCC 3) and thinly populated (RUCC 4) counties. Associations with overall EQI values and class of diabetes prevalence trends differed by RUCC strata, with the clearest association between poor air EQI and steeper increases in diabetes prevalence among rural counties (RUCC 3 and 4).
Conclusions: Similarities in county-level diabetes prevalence trends between 2004 and 2017 were identified for each RUCC strata, although associations with environmental factors varied by rurality.
{"title":"Latent growth trajectories of county-level diabetes prevalence in the United States, 2004-2017, and associations with overall environmental quality.","authors":"Tara P McAlexander, Jyotsna S Jagai, Leslie A McClure","doi":"10.1097/EE9.0000000000000218","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000218","url":null,"abstract":"<p><p>The prevalence of type 2 diabetes (T2D) has increased in the United States, and recent studies suggest that environmental factors contribute to T2D risk. We sought to understand if environmental factors were associated with the rate and magnitude of increase in diabetes prevalence at the county level.</p><p><strong>Methods: </strong>We obtained age-adjusted diabetes prevalence estimates from the CDC for 3,137 US counties from 2004 to 2017. We applied latent growth mixture models to these data to identify classes of counties with similar trends in diabetes prevalence over time, stratified by Rural Urban Continuum Codes (RUCC). We then compared mean values of the US EPA Environmental Quality Index (EQI) 2006-2010, overall and for each of the five domain indices (air, water, land, sociodemographic, and built), with RUCC-specific latent class to examine associations of environmental factors and class of diabetes prevalence trajectory.</p><p><strong>Results: </strong>Overall diabetes prevalence trends between 2004 and 2017 were similar across all RUCC strata. We identified two classes among metropolitan urbanized (RUCC 1) counties; four classes among non-metro urbanized (RUCC 2) counties; and three classes among less urbanized (RUCC 3) and thinly populated (RUCC 4) counties. Associations with overall EQI values and class of diabetes prevalence trends differed by RUCC strata, with the clearest association between poor air EQI and steeper increases in diabetes prevalence among rural counties (RUCC 3 and 4).</p><p><strong>Conclusions: </strong>Similarities in county-level diabetes prevalence trends between 2004 and 2017 were identified for each RUCC strata, although associations with environmental factors varied by rurality.</p>","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2022-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/8b/fb/ee9-6-e218.PMC9374184.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40633127","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-06-01DOI: 10.1097/EE9.0000000000000212
J. Laiho, O. Laitinen, Johannes Malkamäki, L. Puustinen, A. Sinkkonen, J. Pärkkä, H. Hyöty
The incidence of immune-mediated diseases (IMDs) is increasing rapidly in the developed countries constituting a huge medical, economic, and societal challenge. The exposome plays an important role since genetic factors cannot explain such a rapid change. In the Human Exposomic Determinants of Immune Mediated Diseases (HEDIMED) project, altogether 22 academic and industrial partners join their multidisciplinary forces to identify exposomic determinants that are driving the IMD epidemic. The project is based on a combination of data and biological samples from large clinical cohorts constituting about 350,000 pregnant women, 30,000 children prospectively followed from birth, and 7,000 children from cross-sectional studies. HEDIMED focuses on common chronic IMDs that cause a significant disease burden, including type 1 diabetes, celiac disease, allergy, and asthma. Exposomic disease determinants and the underlying biological pathways will be identified by an exploratory approach using advanced omics and multiplex technologies combined with cutting-edge data mining technologies. Emphasis is put on fetal and childhood exposome since the IMD disease processes start early. Inclusion of several IMDs makes it possible to identify common exposomic determinants for the diseases, thus facilitating the development of widely operating preventive and curative treatments. HEDIMED includes data and samples from birth cohorts and clinical trials that have used exposomic interventions and cell and organ culture models to identify mechanisms of the observed associations. Importantly, HEDIMED generates a toolbox that offers science-based functional tools for key stakeholders to control the IMD epidemic. Altogether, HEDIMED aims at innovations, which become widely exploited in diagnostic, therapeutic, preventive, and health economic approaches.
{"title":"Exposomic determinants of immune-mediated diseases","authors":"J. Laiho, O. Laitinen, Johannes Malkamäki, L. Puustinen, A. Sinkkonen, J. Pärkkä, H. Hyöty","doi":"10.1097/EE9.0000000000000212","DOIUrl":"https://doi.org/10.1097/EE9.0000000000000212","url":null,"abstract":"The incidence of immune-mediated diseases (IMDs) is increasing rapidly in the developed countries constituting a huge medical, economic, and societal challenge. The exposome plays an important role since genetic factors cannot explain such a rapid change. In the Human Exposomic Determinants of Immune Mediated Diseases (HEDIMED) project, altogether 22 academic and industrial partners join their multidisciplinary forces to identify exposomic determinants that are driving the IMD epidemic. The project is based on a combination of data and biological samples from large clinical cohorts constituting about 350,000 pregnant women, 30,000 children prospectively followed from birth, and 7,000 children from cross-sectional studies. HEDIMED focuses on common chronic IMDs that cause a significant disease burden, including type 1 diabetes, celiac disease, allergy, and asthma. Exposomic disease determinants and the underlying biological pathways will be identified by an exploratory approach using advanced omics and multiplex technologies combined with cutting-edge data mining technologies. Emphasis is put on fetal and childhood exposome since the IMD disease processes start early. Inclusion of several IMDs makes it possible to identify common exposomic determinants for the diseases, thus facilitating the development of widely operating preventive and curative treatments. HEDIMED includes data and samples from birth cohorts and clinical trials that have used exposomic interventions and cell and organ culture models to identify mechanisms of the observed associations. Importantly, HEDIMED generates a toolbox that offers science-based functional tools for key stakeholders to control the IMD epidemic. Altogether, HEDIMED aims at innovations, which become widely exploited in diagnostic, therapeutic, preventive, and health economic approaches.","PeriodicalId":11713,"journal":{"name":"Environmental Epidemiology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46090956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}