Perfluorooctane sulfonate (PFOS), an industrially synthesized persistent organic pollutant (POP), is intricately intertwined with human production and daily life. It has been discovered that PFOS is related to an elevated incidence of birth defects in fetuses. In contrast, melatonin (MLT), a hormone secreted by the pineal gland, has been demonstrated to exert a protective effect on reproductive development.
Methods
This paper investigates the protective effect of MLT against PFOS-induced reproductive toxicity by simultaneously orally administering MLT to pregnant mice exposed to PFOS. The therapeutic effect was evaluated through the monitoring of pregnancy outcomes, histological changes in the placenta, apoptosis and proliferation of placental spongiotrophoblast, as well as the expression of antioxidant enzyme genes, anti-aging genes, anti-inflammatory genes and other relevant genes.
Results
The results of the study demonstrated that MLT treatment reversed the adverse pregnancy outcomes caused by toxic PFOS, including a low number of implanted fetuses, low neonatal fetal weight, and an increased number of resorbed fetuses. MLT treatment decreased the levels of MDA, an oxidation product generated by PFOS in the placenta of pregnant mice, and increased the levels of the antioxidant enzyme SOD. Additionally, MLT was able to maintain the normalization of placental structure, reduce apoptosis and sustain the proliferation of placental spongiotrophoblast by upregulating the expression of antioxidant genes (Nrf2, CAT) and anti-aging gene (Klotho), anti-inflammatory gene (Hsd11b2), thereby counteracting the oxidative stress caused by PFOS in the placenta, moreover, it also reduced the expression of inflammatory genes (Pycard) in the placenta.
Conclusions
The findings firmly establish the effectiveness of MLT in mitigating the harmful impacts of tainted PFOS on reproductive development during pregnancy. This provides a novel therapeutic approach for addressing PFOS-induced birth defects in fetuses.
{"title":"Melatonin Attenuates PFOS-Induced Reproductive Toxicity of Pregnant Mice due to Placental Damage Via Antioxidant, Anti-Aging and Anti-Inflammatory Pathways","authors":"Jianqiu Han, Zhikai Lu, Yalei Qi, Tengfei Liu, Yongmei Li, Honghui Han, Chen Zhao, Xueyun Ma","doi":"10.1002/bdr2.2423","DOIUrl":"10.1002/bdr2.2423","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Perfluorooctane sulfonate (PFOS), an industrially synthesized persistent organic pollutant (POP), is intricately intertwined with human production and daily life. It has been discovered that PFOS is related to an elevated incidence of birth defects in fetuses. In contrast, melatonin (MLT), a hormone secreted by the pineal gland, has been demonstrated to exert a protective effect on reproductive development.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This paper investigates the protective effect of MLT against PFOS-induced reproductive toxicity by simultaneously orally administering MLT to pregnant mice exposed to PFOS. The therapeutic effect was evaluated through the monitoring of pregnancy outcomes, histological changes in the placenta, apoptosis and proliferation of placental spongiotrophoblast, as well as the expression of antioxidant enzyme genes, anti-aging genes, anti-inflammatory genes and other relevant genes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The results of the study demonstrated that MLT treatment reversed the adverse pregnancy outcomes caused by toxic PFOS, including a low number of implanted fetuses, low neonatal fetal weight, and an increased number of resorbed fetuses. MLT treatment decreased the levels of MDA, an oxidation product generated by PFOS in the placenta of pregnant mice, and increased the levels of the antioxidant enzyme SOD. Additionally, MLT was able to maintain the normalization of placental structure, reduce apoptosis and sustain the proliferation of placental spongiotrophoblast by upregulating the expression of antioxidant genes (Nrf2, CAT) and anti-aging gene (Klotho), anti-inflammatory gene (Hsd11b2), thereby counteracting the oxidative stress caused by PFOS in the placenta, moreover, it also reduced the expression of inflammatory genes (Pycard) in the placenta.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The findings firmly establish the effectiveness of MLT in mitigating the harmful impacts of tainted PFOS on reproductive development during pregnancy. This provides a novel therapeutic approach for addressing PFOS-induced birth defects in fetuses.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9121,"journal":{"name":"Birth Defects Research","volume":"116 12","pages":""},"PeriodicalIF":1.6,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11635750/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142811879","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sarah C. Fisher, Paul A. Romitti, Melissa Tracy, Meredith M. Howley, Ethylin Wang Jabs, Marilyn L. Browne, the National Birth Defects Prevention Study
Background
Previous studies of maternal alcohol consumption and craniosynostosis have reported null or inverse associations. We updated a previous analysis of National Birth Defects Prevention Study (NBDPS) data to further examine associations between maternal alcohol consumption and craniosynostosis.
Methods
NBDPS was a multi-site, population-based case–control study. Mothers of craniosynostosis cases and randomly selected liveborn controls delivered during 1997–2011 completed a telephone interview about pregnancy exposures. We examined associations for self-reported periconceptional maternal alcohol consumption (during the month before conception through the third gestational month) and odds of craniosynostosis in offspring. We used logistic regression to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for associations between any alcohol consumption and binge consumption and craniosynostosis, overall and by affected suture. Finally, we performed a probabilistic bias analysis using a range of assumptions about the sensitivity and specificity of self-reported consumption by case/control status.
Results
We analyzed interview data from 1435 mothers of craniosynostosis cases and 11,216 mothers of controls. Periconceptional alcohol consumption prevalence was similar among case (36.9%) and control (38.2%) mothers. We observed point estimates near or below 1.0 for alcohol consumption (any and binge) and all suture subtypes of craniosynostosis, with all CIs including the null. Our bias-adjusted estimates for periconceptional alcohol consumption were higher than our conventional estimates but supported the null findings.
Conclusions
We observed primarily null associations between maternal periconceptional alcohol consumption and craniosynostosis. However, our findings do not diminish the prevailing clinical guidance in the United States that pregnant people should abstain from alcohol consumption.
{"title":"Associations Between Maternal Periconceptional Alcohol Consumption and Risk of Craniosynostosis Among Offspring, National Birth Defects Prevention Study, 1997–2011","authors":"Sarah C. Fisher, Paul A. Romitti, Melissa Tracy, Meredith M. Howley, Ethylin Wang Jabs, Marilyn L. Browne, the National Birth Defects Prevention Study","doi":"10.1002/bdr2.2420","DOIUrl":"10.1002/bdr2.2420","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Previous studies of maternal alcohol consumption and craniosynostosis have reported null or inverse associations. We updated a previous analysis of National Birth Defects Prevention Study (NBDPS) data to further examine associations between maternal alcohol consumption and craniosynostosis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>NBDPS was a multi-site, population-based case–control study. Mothers of craniosynostosis cases and randomly selected liveborn controls delivered during 1997–2011 completed a telephone interview about pregnancy exposures. We examined associations for self-reported periconceptional maternal alcohol consumption (during the month before conception through the third gestational month) and odds of craniosynostosis in offspring. We used logistic regression to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for associations between any alcohol consumption and binge consumption and craniosynostosis, overall and by affected suture. Finally, we performed a probabilistic bias analysis using a range of assumptions about the sensitivity and specificity of self-reported consumption by case/control status.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We analyzed interview data from 1435 mothers of craniosynostosis cases and 11,216 mothers of controls. Periconceptional alcohol consumption prevalence was similar among case (36.9%) and control (38.2%) mothers. We observed point estimates near or below 1.0 for alcohol consumption (any and binge) and all suture subtypes of craniosynostosis, with all CIs including the null. Our bias-adjusted estimates for periconceptional alcohol consumption were higher than our conventional estimates but supported the null findings.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>We observed primarily null associations between maternal periconceptional alcohol consumption and craniosynostosis. However, our findings do not diminish the prevailing clinical guidance in the United States that pregnant people should abstain from alcohol consumption.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9121,"journal":{"name":"Birth Defects Research","volume":"116 12","pages":""},"PeriodicalIF":1.6,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142811878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Nahed O. ElHassan, Ruiqi Cen, Charles P. Pugh, Chary Akmyradov, Jun Ying, Anthony Goudie, Wendy N. Nembhard
Background
There are limited studies on educational outcomes of children born with esophageal atresia (EA) with or without tracheoesophageal fistula (TEF). We aimed to compare 3rd to 5th grade academic proficiency among children born with EA/TEF versus unaffected children.
Methods
Children born with EA/TEF (2000–2005) were identified from the Arkansas Reproductive Health Monitoring System. For each child born with EA/TEF, up to two unaffected children were selected from birth certificates and matched on hospital and month of birth, sex, and race and ethnicity. Data on NICU hospitalization were abstracted from medical records at Arkansas' only pediatric specialty hospital. The study outcomes were 3rd to 5th grade proficiency on literacy and mathematic standardized achievement tests, referral to special education, and days of school absence. Regression models were used to assess the association of outcome measures with diagnosis of EA/TEF, after adjusting for differences in covariates between EA/TEF and unaffected children and accounting for paired correlations using the generalized estimating equation method.
Results
The final cohort included 20 surviving children born with EA/TEF and 31 unaffected children. There was no significant difference in literacy (3rd: 70% vs. 71%; 4th: 83% vs. 81%; 5th: 94% vs. 87%, p > 0.05) or mathematics proficiency (3rd: 80% vs. 87%; 4th: 83% vs. 78%; 5th: 75% vs. 78%, p > 0.05), referral to special education (20% vs. 19%, p = 0.65), or total days of school absence (47 vs. 26 days, p = 0.07) between EA/TEF and unaffected children.
Conclusions
Children born with EA/TEF had comparable academic proficiency to unaffected children.
背景：关于先天性食管闭锁（EA）患儿伴或不伴气管食管瘘（TEF）的教育效果的研究有限。我们的目的是比较出生时患有EA/TEF的儿童与未受影响的儿童的三年级到五年级的学术水平。方法：从阿肯色州生殖健康监测系统中确定2000-2005年出生时患有EA/TEF的儿童。对于每个出生时患有EA/TEF的儿童，从出生证明中选择最多两个未受影响的儿童，并根据医院和出生月份、性别、种族和民族进行匹配。新生儿重症监护病房住院的数据是从阿肯色州唯一一家儿科专科医院的医疗记录中提取的。研究结果包括三到五年级的读写和数学标准化成绩测试的熟练程度，转到特殊教育的情况，以及缺课天数。在调整EA/TEF和未受影响儿童之间协变量的差异，并使用广义估计方程方法考虑配对相关性后，使用回归模型评估结果测量与EA/TEF诊断的相关性。结果：最终队列包括20名出生时患有EA/TEF的幸存儿童和31名未受影响的儿童。在读写能力方面没有显著差异(第三：70% vs 71%；第4:83% vs. 81%；第五名：94% vs. 87%, p > 0.05)或数学熟练程度(第三名：80% vs. 87%；第4:83% vs. 78%；第5:75%对78%，p > 0.05)，转到特殊教育（20%对19%，p = 0.65），或总缺课天数（47对26天，p = 0.07）在EA/TEF和未受影响的儿童之间。结论：出生时患有EA/TEF的儿童与未受影响的儿童具有相当的学术熟练程度。
{"title":"Childhood Educational Outcomes of Infants Born With Esophageal Atresia With or Without Tracheoesophageal Atresia","authors":"Nahed O. ElHassan, Ruiqi Cen, Charles P. Pugh, Chary Akmyradov, Jun Ying, Anthony Goudie, Wendy N. Nembhard","doi":"10.1002/bdr2.2417","DOIUrl":"10.1002/bdr2.2417","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>There are limited studies on educational outcomes of children born with esophageal atresia (EA) with or without tracheoesophageal fistula (TEF). We aimed to compare 3rd to 5th grade academic proficiency among children born with EA/TEF versus unaffected children.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Children born with EA/TEF (2000–2005) were identified from the Arkansas Reproductive Health Monitoring System. For each child born with EA/TEF, up to two unaffected children were selected from birth certificates and matched on hospital and month of birth, sex, and race and ethnicity. Data on NICU hospitalization were abstracted from medical records at Arkansas' only pediatric specialty hospital. The study outcomes were 3rd to 5th grade proficiency on literacy and mathematic standardized achievement tests, referral to special education, and days of school absence. Regression models were used to assess the association of outcome measures with diagnosis of EA/TEF, after adjusting for differences in covariates between EA/TEF and unaffected children and accounting for paired correlations using the generalized estimating equation method.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The final cohort included 20 surviving children born with EA/TEF and 31 unaffected children. There was no significant difference in literacy (3rd: 70% vs. 71%; 4th: 83% vs. 81%; 5th: 94% vs. 87%, p > 0.05) or mathematics proficiency (3rd: 80% vs. 87%; 4th: 83% vs. 78%; 5th: 75% vs. 78%, <i>p</i> > 0.05), referral to special education (20% vs. 19%, <i>p</i> = 0.65), or total days of school absence (47 vs. 26 days, <i>p</i> = 0.07) between EA/TEF and unaffected children.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Children born with EA/TEF had comparable academic proficiency to unaffected children.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9121,"journal":{"name":"Birth Defects Research","volume":"116 12","pages":""},"PeriodicalIF":1.6,"publicationDate":"2024-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142794232","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A meta-analysis of case-control studies was conducted to assess the risk of birth defects in offspring in China associated with maternal active and passive smoking and paternal smoking.
Methods
Four electronic databases were searched for qualified research up to December 2023. A Random-effect model or fixed-effect model was used to calculate the overall comprehensive risk estimates; and the relationship between parental smoking and the risk of birth defects in different periods of pregnancy. Subgroup and sensitivity analyses were performed to explore possible sources of heterogeneity.
Results
Sixty-two qualified studies involving 137,574 cases and 8,770,837 controls were included. Overall, maternal active smoking (OR = 2.19; 95% confidence interval (CI): 1.72–2.79; p < 0.01) and passive smoking (OR = 2.59,95% CI: 2.24–2.99; p < 0.01) as well as paternal active smoking (OR = 1.47,95% CI: 1.34–1.62; p < 0.01) were significantly associated with birth defect risk. The sources of heterogeneity were explored by subgroup analysis. Subgroup analysis showed that the risk of congenital heart disease in offspring was increased in paternal and maternal active smoking (OR = 2.97, 95% CI: 2.01–4.39; OR = 1.51, 95% CI: 1.30–1.74), respectively. Sensitivity analysis yielded consistent results.
Conclusion
Maternal active and passive smoking and paternal active smoking are risk factors for birth defects in offspring. Parents should be encouraged to quit smoking during the perinatal period and pregnancy.
{"title":"Parental Smoking and the Risk of Birth Defects in Offspring in China: A Systematic Review and meta-Analysis","authors":"Jinxi Han, Yunxia Zhang, Yibo Liu, Jikai Liu, Yuehua Zhang, Kaijuan Wang","doi":"10.1002/bdr2.2422","DOIUrl":"10.1002/bdr2.2422","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>A meta-analysis of case-control studies was conducted to assess the risk of birth defects in offspring in China associated with maternal active and passive smoking and paternal smoking.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Four electronic databases were searched for qualified research up to December 2023. A Random-effect model or fixed-effect model was used to calculate the overall comprehensive risk estimates; and the relationship between parental smoking and the risk of birth defects in different periods of pregnancy. Subgroup and sensitivity analyses were performed to explore possible sources of heterogeneity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Sixty-two qualified studies involving 137,574 cases and 8,770,837 controls were included. Overall, maternal active smoking (OR = 2.19; 95% confidence interval (CI): 1.72–2.79; <i>p</i> < 0.01) and passive smoking (OR = 2.59,95% CI: 2.24–2.99; <i>p</i> < 0.01) as well as paternal active smoking (OR = 1.47,95% CI: 1.34–1.62; <i>p</i> < 0.01) were significantly associated with birth defect risk. The sources of heterogeneity were explored by subgroup analysis. Subgroup analysis showed that the risk of congenital heart disease in offspring was increased in paternal and maternal active smoking (OR = 2.97, 95% CI: 2.01–4.39; OR = 1.51, 95% CI: 1.30–1.74), respectively. Sensitivity analysis yielded consistent results.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Maternal active and passive smoking and paternal active smoking are risk factors for birth defects in offspring. Parents should be encouraged to quit smoking during the perinatal period and pregnancy.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9121,"journal":{"name":"Birth Defects Research","volume":"116 12","pages":""},"PeriodicalIF":1.6,"publicationDate":"2024-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142794256","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Waheed Ahmad, Muhammad Ali Kanwal, Iram Inayat, Syeda Nadia Ahmad, Aima Iram Batool, Nazish Ghazanfar, Rabia Idrees, Sadia Suleman, Asma Younis, Khawaja Raees Ahmad
Background
Heavy metals like lead (Pb) have been used by humans for a very long time, but throughout the industrial revolution, their use expanded, increasing exposure to the metal. Lead, however, has no biological purpose in the human body and is hazardous when it gets into soft tissues and organs. Lead is still used in a variety of industries, including battery manufacturing and car maintenance, despite efforts to limit its usage.
Objective
This study investigates the teratogenic and morphometric effects of lead on chick embryos and the potential ameliorative effects of vitamin B6.
Methods
Two hundred fertilized eggs from the golden black chicken were divided into four groups: control, lead acetate, vitamin B6, and lead + vitamin B6.
Results
On the 14th day, embryos were analyzed. Significant reductions in body weight and size were observed in the lead-exposed group (33.93 ± 1.27 g) compared to the control (41.12 ± 0.97 g). Pronounced deformities included rudimentary beaks, protruding eyes, tridactyl limbs, hydrocephaly, and neck deformities. Appendicular deformities like phocomelia, amelia, and abnormal phalanges growth were also noted. Vitamin B6 demonstrated therapeutic benefits, significantly improving mean embryo weight in the Lead + Vitamin B6 group (42.37 ± 0.99 g). The lead-exposed group showed a reduction in maxilla length (3.61 ± 1.30 mm) compared to the Lead + Vitamin B6 group (7.57 ± 0.79 mm). This group also showed reduced severity of muscular dystrophy and bone thinning, with signs of recovery in beak and bone sizes.
Conclusions
The study highlights vitamin B6's beneficial impact in mitigating lead's toxic effects on chick embryonic development.
{"title":"Protective Role of Vitamin B6 Against Teratogenic Effects Induced by Lead in Chick Embryo","authors":"Waheed Ahmad, Muhammad Ali Kanwal, Iram Inayat, Syeda Nadia Ahmad, Aima Iram Batool, Nazish Ghazanfar, Rabia Idrees, Sadia Suleman, Asma Younis, Khawaja Raees Ahmad","doi":"10.1002/bdr2.2416","DOIUrl":"10.1002/bdr2.2416","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Heavy metals like lead (Pb) have been used by humans for a very long time, but throughout the industrial revolution, their use expanded, increasing exposure to the metal. Lead, however, has no biological purpose in the human body and is hazardous when it gets into soft tissues and organs. Lead is still used in a variety of industries, including battery manufacturing and car maintenance, despite efforts to limit its usage.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This study investigates the teratogenic and morphometric effects of lead on chick embryos and the potential ameliorative effects of vitamin B6.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Two hundred fertilized eggs from the golden black chicken were divided into four groups: control, lead acetate, vitamin B6, and lead + vitamin B6.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>On the 14th day, embryos were analyzed. Significant reductions in body weight and size were observed in the lead-exposed group (33.93 ± 1.27 g) compared to the control (41.12 ± 0.97 g). Pronounced deformities included rudimentary beaks, protruding eyes, tridactyl limbs, hydrocephaly, and neck deformities. Appendicular deformities like phocomelia, amelia, and abnormal phalanges growth were also noted. Vitamin B6 demonstrated therapeutic benefits, significantly improving mean embryo weight in the Lead + Vitamin B6 group (42.37 ± 0.99 g). The lead-exposed group showed a reduction in maxilla length (3.61 ± 1.30 mm) compared to the Lead + Vitamin B6 group (7.57 ± 0.79 mm). This group also showed reduced severity of muscular dystrophy and bone thinning, with signs of recovery in beak and bone sizes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The study highlights vitamin B6's beneficial impact in mitigating lead's toxic effects on chick embryonic development.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9121,"journal":{"name":"Birth Defects Research","volume":"116 12","pages":""},"PeriodicalIF":1.6,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142715365","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Charlotte Dubucs, Anthony Caillet, Félix Frémont, Laurane Delteil, Van N'Go, Amanda Julie Neville, Elisa Ballardini, Helen Dolk, Maria Loane, Ester Garne, Babak Khoshnood, Nathalie Lelong, Anke Rissmann, Mary O'Mahony, Anna Pierini, Miriam Gatt, Jorieke Bergman, Maciej Robert Krawczynski, Anna Latos Bielenska, Luis Javier Echevarría González de Garibay, Clara Cavero-Carbonell, Marie-Claude Addor, David Tucker, Sue Jordan, Elly Den Hond, Vera Nelen, Ingeborg Barisic, Florence Rouget, Hanitra Randrianaivo, Jonathan Hoareau, Isabelle Perthus, Caroline Hurault-Delarue, Monique Courtade-Saïdi, Christine Damase-Michel
Background
Congenital ocular anomalies (COA) are among the most common causes of visual impairment in children in high-income countries. The aim of the study is to describe the prevalence of the various COA recorded in European population-based registries of CA (EUROCAT) participating in the EUROmediCAT consortium.
Methods
Data from 19 EUROmediCAT registries and one healthcare database (EFEMERIS) were included in this descriptive epidemiological study. Cases of COA included live births, FD from 20 weeks gestational age (GA), and termination of pregnancy for fetal anomaly.
Results
The prevalence of total COA was 3.47/10,000 births (95% CI [3.61–3.82]), ranging from 1.41 to 13.46/10,000 depending on the registry. Among COA cases, congenital lens anomalies were the most frequent anomalies (31%), of which over half were single ocular anomalies (presenting with only one ocular anomaly). An/microphthalmia was the second most frequent COA (24%) of which three-quarters were multiply malformed (associated to extraocular major anomalies). Among single COA cases, 58 were prenatally diagnosed (4%), of which, 58% were diagnosed in the second trimester. Known genetic causes of COA explained 2.5%–25% of COA depending on their class.
Conclusions
This is the first European study describing COA. The detailed prevalence data offered in this study could improve screening and early diagnosis of different classes of COA. As COA are rare, epidemiological surveillance of large populations and accurate clinical descriptions are essential.
背景 先天性眼部异常（COA）是高收入国家儿童视力受损的最常见原因之一。本研究旨在描述参与 EUROmediCAT 联盟的欧洲人群先天性视力异常登记处（EUROCAT）所记录的各种先天性视力异常的发病率。 方法 这项描述性流行病学研究纳入了来自 19 个 EUROmediCAT 登记处和一个医疗保健数据库（EFEMERIS）的数据。COA病例包括活产、胎龄20周以上的胎儿畸形和因胎儿畸形而终止妊娠。 结果 COA 的总患病率为 3.47/10,000（95% CI [3.61-3.82]），根据登记册的不同，患病率从 1.41 到 13.46/10,000 不等。在 COA 病例中，先天性晶状体异常是最常见的异常（31%），其中一半以上是单眼异常（仅出现一种眼部异常）。无/小眼症是第二常见的先天性角膜异常（24%），其中四分之三是多发性畸形（与眼外大畸形有关）。在单个 COA 病例中，58 例是产前诊断的（4%），其中 58% 是在怀孕后三个月诊断的。已知的 COA 遗传原因占 COA 的 2.5%-25%，具体取决于其类别。 结论 这是欧洲第一项描述 COA 的研究。该研究提供的详细发病率数据可改善不同类别 COA 的筛查和早期诊断。由于 COA 非常罕见，因此对大量人群进行流行病学监测和准确的临床描述至关重要。
{"title":"Prevalence of Congenital Ocular Anomalies in 15 Countries of Europe: Results From the Medikeye Study","authors":"Charlotte Dubucs, Anthony Caillet, Félix Frémont, Laurane Delteil, Van N'Go, Amanda Julie Neville, Elisa Ballardini, Helen Dolk, Maria Loane, Ester Garne, Babak Khoshnood, Nathalie Lelong, Anke Rissmann, Mary O'Mahony, Anna Pierini, Miriam Gatt, Jorieke Bergman, Maciej Robert Krawczynski, Anna Latos Bielenska, Luis Javier Echevarría González de Garibay, Clara Cavero-Carbonell, Marie-Claude Addor, David Tucker, Sue Jordan, Elly Den Hond, Vera Nelen, Ingeborg Barisic, Florence Rouget, Hanitra Randrianaivo, Jonathan Hoareau, Isabelle Perthus, Caroline Hurault-Delarue, Monique Courtade-Saïdi, Christine Damase-Michel","doi":"10.1002/bdr2.2414","DOIUrl":"https://doi.org/10.1002/bdr2.2414","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Congenital ocular anomalies (COA) are among the most common causes of visual impairment in children in high-income countries. The aim of the study is to describe the prevalence of the various COA recorded in European population-based registries of CA (EUROCAT) participating in the EUROmediCAT consortium.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Data from 19 EUROmediCAT registries and one healthcare database (EFEMERIS) were included in this descriptive epidemiological study. Cases of COA included live births, FD from 20 weeks gestational age (GA), and termination of pregnancy for fetal anomaly.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The prevalence of total COA was 3.47/10,000 births (95% CI [3.61–3.82]), ranging from 1.41 to 13.46/10,000 depending on the registry. Among COA cases, congenital lens anomalies were the most frequent anomalies (31%), of which over half were single ocular anomalies (presenting with only one ocular anomaly). An/microphthalmia was the second most frequent COA (24%) of which three-quarters were multiply malformed (associated to extraocular major anomalies). Among single COA cases, 58 were prenatally diagnosed (4%), of which, 58% were diagnosed in the second trimester. Known genetic causes of COA explained 2.5%–25% of COA depending on their class.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>This is the first European study describing COA. The detailed prevalence data offered in this study could improve screening and early diagnosis of different classes of COA. As COA are rare, epidemiological surveillance of large populations and accurate clinical descriptions are essential.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9121,"journal":{"name":"Birth Defects Research","volume":"116 11","pages":""},"PeriodicalIF":1.6,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/bdr2.2414","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142708355","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Rachel P. Allred, J. Aguilar-Martinez, R. Howell, Dayana Betancourt, Lisa Marengo, A. Dixon, H. Jeon, C. Yantz, M. Kilburn, Margaret Drummond-Borg, Joanne Nguyen, Fernando Arena, Charles Shumate
<div> <section> <h3> Background</h3> <p>Macrocephaly is a clinical observation denoted as an occipitofrontal head circumference exceeding two standard deviations above same age and sex norms. By its definition, macrocephaly occurs in approximately 3% of the population. Descriptive epidemiologic evaluations of macrocephaly are lacking in the literature. The primary objective of this study was to describe the prevalence of macrocephaly captured by the Texas Birth Defects Registry (TBDR) by infant sex, rural/urban residence, and select maternal characteristics.</p> </section> <section> <h3> Methods</h3> <p>Cases of TBDR between 1999 and 2019 with a six-digit Centers for Disease Control modified-British Pediatric Association (BPA) code of 742.400 (enlarged brain/head, large head, macrocephaly, megalencephaly) were identified. All pregnancy outcomes and diagnostic certainties were included. Prevalence (per 10,000 live births) and 95% confidence intervals (CIs) were calculated using a Poisson table by rural/urban residence, infant sex, maternal age, education, race/ethnicity, history of diabetes, and body mass index (BMI). Prevalence calculations were repeated across multiple sensitivity analyses including (1) definite, isolated cases excluding those with indication of being either “benign” or “familial”, (2) definite, non-isolated cases, (3) definite non-isolated cases excluding chromosomal and syndromic cases, and (4) definite, proportionate (at birth) cases. A secondary objective was to describe the most common co-occurring congenital defects among definite, non-isolated cases.</p> </section> <section> <h3> Results</h3> <p>Overall, between 1999 and 2019, 14,637 cases of macrocephaly were identified in the TBDR resulting in a prevalence of 18.12/10,000 live births (95% CI: 17.83–18.42). Most cases were live born (99%), had a definite diagnosis (87%), and were non-isolated (57%). Prevalence was significantly higher among males, among those with an urban residence, and among mothers who were older, Non-Hispanic White, who had greater than high school education, who had a history of diabetes, and who were obese. Prevalence patterns remained consistent across all sensitivity analyses. The most common co-occurring congenital defects among definite, non-isolated cases were minor and primarily included skull and facial bone anomalies (e.g., plagiocephaly [18%]).</p> </section> <section> <h3> Conclusions</h3> <p>To our knowledge, this is the first epidemiologic evaluation of macrocephaly in a birth defects registry. The long-term clinical impact of isolated macrocephaly is not well understood and should be the focus of future investigations.<
{"title":"Epidemiology of Macrocephaly in the Texas Birth Defects Registry, 1999–2019","authors":"Rachel P. Allred, J. Aguilar-Martinez, R. Howell, Dayana Betancourt, Lisa Marengo, A. Dixon, H. Jeon, C. Yantz, M. Kilburn, Margaret Drummond-Borg, Joanne Nguyen, Fernando Arena, Charles Shumate","doi":"10.1002/bdr2.2415","DOIUrl":"https://doi.org/10.1002/bdr2.2415","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Macrocephaly is a clinical observation denoted as an occipitofrontal head circumference exceeding two standard deviations above same age and sex norms. By its definition, macrocephaly occurs in approximately 3% of the population. Descriptive epidemiologic evaluations of macrocephaly are lacking in the literature. The primary objective of this study was to describe the prevalence of macrocephaly captured by the Texas Birth Defects Registry (TBDR) by infant sex, rural/urban residence, and select maternal characteristics.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Cases of TBDR between 1999 and 2019 with a six-digit Centers for Disease Control modified-British Pediatric Association (BPA) code of 742.400 (enlarged brain/head, large head, macrocephaly, megalencephaly) were identified. All pregnancy outcomes and diagnostic certainties were included. Prevalence (per 10,000 live births) and 95% confidence intervals (CIs) were calculated using a Poisson table by rural/urban residence, infant sex, maternal age, education, race/ethnicity, history of diabetes, and body mass index (BMI). Prevalence calculations were repeated across multiple sensitivity analyses including (1) definite, isolated cases excluding those with indication of being either “benign” or “familial”, (2) definite, non-isolated cases, (3) definite non-isolated cases excluding chromosomal and syndromic cases, and (4) definite, proportionate (at birth) cases. A secondary objective was to describe the most common co-occurring congenital defects among definite, non-isolated cases.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Overall, between 1999 and 2019, 14,637 cases of macrocephaly were identified in the TBDR resulting in a prevalence of 18.12/10,000 live births (95% CI: 17.83–18.42). Most cases were live born (99%), had a definite diagnosis (87%), and were non-isolated (57%). Prevalence was significantly higher among males, among those with an urban residence, and among mothers who were older, Non-Hispanic White, who had greater than high school education, who had a history of diabetes, and who were obese. Prevalence patterns remained consistent across all sensitivity analyses. The most common co-occurring congenital defects among definite, non-isolated cases were minor and primarily included skull and facial bone anomalies (e.g., plagiocephaly [18%]).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>To our knowledge, this is the first epidemiologic evaluation of macrocephaly in a birth defects registry. The long-term clinical impact of isolated macrocephaly is not well understood and should be the focus of future investigations.<","PeriodicalId":9121,"journal":{"name":"Birth Defects Research","volume":"116 11","pages":""},"PeriodicalIF":1.6,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142708357","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Madeline K. M. Vera-Colón, Gredia Huerta-Montañez, Vijaya Kancherla, Martina Anto-Ocrah, Michelle Myer, Marilyn Helen Silva
Background
High-risk pregnancies and birth defects are often greater within communities of color where resources for a healthy pregnancy are generally lacking. Infant and maternal mortality, preterm birth, and instances of increased developmental and physical defects are related to environmental exposures (e.g., pesticides, lead in water, wildfire smoke), dietary additives, and lack of access to adequate healthcare. More frequently people of color and other under-served groups, are affected by historical inequality and unconscious bias. Compounding these disparities, research into these issues and efforts to address them are poorly supported.
Methods
The speakers in this symposium presented evidence for health disparities within communities of color to foster research aimed at identifying toxic levels of potentially hazardous dietary chemicals, or exposures in the pediatric population can focus on addressing the current inadequacy of translating scientific findings into enforceable policies.
Results
The disparities discussed within this symposium highlighted key areas in desperate need of policy reform. In the United States, regulatory exposure levels have been established for lead exposures but frequently exceed these limits without mitigation. Neural tube defects can be prevented by a simple dietary solution such as fortification of staple foods with folic acid. Recent literature on gender as a social determinant of health has determined women suffer more negative health consequences due to social attitudes.
Conclusions
Ultimately, this symposium provided an understanding of the experience of disadvantaged and marginalized persons during pregnancy, illustrated the disparities that exist in reproductive health, and described the need to address and prevent them.
{"title":"Society for Birth Defects Research and Prevention Symposium: Health Disparities Within Communities of Color","authors":"Madeline K. M. Vera-Colón, Gredia Huerta-Montañez, Vijaya Kancherla, Martina Anto-Ocrah, Michelle Myer, Marilyn Helen Silva","doi":"10.1002/bdr2.2412","DOIUrl":"10.1002/bdr2.2412","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>High-risk pregnancies and birth defects are often greater within communities of color where resources for a healthy pregnancy are generally lacking. Infant and maternal mortality, preterm birth, and instances of increased developmental and physical defects are related to environmental exposures (e.g., pesticides, lead in water, wildfire smoke), dietary additives, and lack of access to adequate healthcare. More frequently people of color and other under-served groups, are affected by historical inequality and unconscious bias. Compounding these disparities, research into these issues and efforts to address them are poorly supported.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The speakers in this symposium presented evidence for health disparities within communities of color to foster research aimed at identifying toxic levels of potentially hazardous dietary chemicals, or exposures in the pediatric population can focus on addressing the current inadequacy of translating scientific findings into enforceable policies.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The disparities discussed within this symposium highlighted key areas in desperate need of policy reform. In the United States, regulatory exposure levels have been established for lead exposures but frequently exceed these limits without mitigation. Neural tube defects can be prevented by a simple dietary solution such as fortification of staple foods with folic acid. Recent literature on gender as a social determinant of health has determined women suffer more negative health consequences due to social attitudes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Ultimately, this symposium provided an understanding of the experience of disadvantaged and marginalized persons during pregnancy, illustrated the disparities that exist in reproductive health, and described the need to address and prevent them.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9121,"journal":{"name":"Birth Defects Research","volume":"116 11","pages":""},"PeriodicalIF":1.6,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142614519","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Danielle L. Mitchell, Tiffany M. Chambers, A. J. Agopian, Renata H. Benjamin, Charles J. Shumate, Anne Slavotinek, Robert B. Hufnagel, Brian P. Brooks, Laura E. Mitchell, Philip J. Lupo
Background
Coloboma is a rare congenital malformation in which part of the tissue that makes up the eye is missing and may cause visual impairment or blindness. Little is known about the epidemiology of this condition. Therefore, we obtained data from the Texas Birth Defects Registry on children identified with coloboma for the period 1999–2014.
Methods
Using information on all live births from the same period, prevalence ratios (PRs) for selected demographic and clinical factors were used to estimate associations using Poisson regression among cases with coloboma. Coloboma cases were divided into subgroups to explore patterns of co-occurring defects and syndromes. All variables significant in unadjusted models (p < 0.05) were included in multivariable models to evaluate adjusted PRs (aPRs).
Results
We identified 1587 cases with coloboma, of whom 934 (58.8%) were nonsyndromic, and 474 (29.9%) were isolated. When considering all identified cases, factors associated with significant differences in prevalence included plurality (multiple vs. singleton aPR = 1.4, 95% CI: 1.1–1.8); maternal education (college or greater vs. less than high school aPR = 0.7, 95% CI: 0.6–0.9); maternal race/ethnicity (Hispanic vs. non-Hispanic White aPR = 0.9, 95% CI: 0.8–1.0); and maternal diabetes (yes vs. no aPR = 1.3, 95% CI: 1.0–1.6). There was a notable increase in the birth prevalence of coloboma during the study period (p-for-trend < 0.001). Effect estimates were similar across the different subgroups.
Conclusion
In our large population, we identified several factors associated with the prevalence of coloboma. These findings may help define subgroups of women more likely to have children affected by coloboma, which could inform improved screening efforts.
{"title":"Epidemiology of Coloboma: Prevalence and Patterns in Texas, 1999–2014","authors":"Danielle L. Mitchell, Tiffany M. Chambers, A. J. Agopian, Renata H. Benjamin, Charles J. Shumate, Anne Slavotinek, Robert B. Hufnagel, Brian P. Brooks, Laura E. Mitchell, Philip J. Lupo","doi":"10.1002/bdr2.2413","DOIUrl":"10.1002/bdr2.2413","url":null,"abstract":"<div>\u0000 <section>\u0000 <h3> Background</h3>\u0000 <p>Coloboma is a rare congenital malformation in which part of the tissue that makes up the eye is missing and may cause visual impairment or blindness. Little is known about the epidemiology of this condition. Therefore, we obtained data from the Texas Birth Defects Registry on children identified with coloboma for the period 1999–2014.</p>\u0000 </section>\u0000 <section>\u0000 <h3> Methods</h3>\u0000 <p>Using information on all live births from the same period, prevalence ratios (PRs) for selected demographic and clinical factors were used to estimate associations using Poisson regression among cases with coloboma. Coloboma cases were divided into subgroups to explore patterns of co-occurring defects and syndromes. All variables significant in unadjusted models (<i>p</i> < 0.05) were included in multivariable models to evaluate adjusted PRs (aPRs).</p>\u0000 </section> \u0000 <section>\u0000 <h3> Results</h3>\u0000 <p>We identified 1587 cases with coloboma, of whom 934 (58.8%) were nonsyndromic, and 474 (29.9%) were isolated. When considering all identified cases, factors associated with significant differences in prevalence included plurality (multiple vs. singleton aPR = 1.4, 95% CI: 1.1–1.8); maternal education (college or greater vs. less than high school aPR = 0.7, 95% CI: 0.6–0.9); maternal race/ethnicity (Hispanic vs. non-Hispanic White aPR = 0.9, 95% CI: 0.8–1.0); and maternal diabetes (yes vs. no aPR = 1.3, 95% CI: 1.0–1.6). There was a notable increase in the birth prevalence of coloboma during the study period (<i>p</i>-for-trend < 0.001). Effect estimates were similar across the different subgroups.</p>\u0000 </section>\u0000 <section>\u0000 <h3> Conclusion</h3>\u0000 <p>In our large population, we identified several factors associated with the prevalence of coloboma. These findings may help define subgroups of women more likely to have children affected by coloboma, which could inform improved screening efforts.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9121,"journal":{"name":"Birth Defects Research","volume":"116 11","pages":""},"PeriodicalIF":1.6,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142614498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Tobacco smoke has a global impact, particularly on pregnant women and their newborns. An emerging body of research suggests that passive tobacco smoking is a significant contributor to congenital cardiovascular disorders (CVDs).
Aim of the Study
This study aimed to mimic the effects of passive tobacco smoke (PTS) on neonates exposed throughout the gestational period.
Methods
Female mice (DPC = 0) were exposed to PTS; 24 cigarettes/day with an interval of 10 min between each cigarette in a specialized smoke chamber from conception to birth. Histopathological analysis was employed to evaluate PTS-induced cardiac damage in neonates.
Results
The results revealed significant alterations in cell structure, namely, widened interstitial spaces, hemorrhage, pyknotic nuclei, inflammatory cell infiltration, collagen deposition, and fibrosis.
Conclusion
Maternal exposure to PTS during pregnancy may lead to neonatal myocardiopathy.
{"title":"The Impact of Maternal Passive Tobacco Smoke on Neonatal Myocardiopathy in Mice","authors":"Naseer Kawish, Muddasir Hassan Abbasi, Muhammad Babar Khawar, Tasleem Akhtar, Amin Arif, Ayesha Majid, Nadeem Sheikh","doi":"10.1002/bdr2.2411","DOIUrl":"10.1002/bdr2.2411","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Tobacco smoke has a global impact, particularly on pregnant women and their newborns. An emerging body of research suggests that passive tobacco smoking is a significant contributor to congenital cardiovascular disorders (CVDs).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Aim of the Study</h3>\u0000 \u0000 <p>This study aimed to mimic the effects of passive tobacco smoke (PTS) on neonates exposed throughout the gestational period.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Female mice (DPC = 0) were exposed to PTS; 24 cigarettes/day with an interval of 10 min between each cigarette in a specialized smoke chamber from conception to birth. Histopathological analysis was employed to evaluate PTS-induced cardiac damage in neonates.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The results revealed significant alterations in cell structure, namely, widened interstitial spaces, hemorrhage, pyknotic nuclei, inflammatory cell infiltration, collagen deposition, and fibrosis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Maternal exposure to PTS during pregnancy may lead to neonatal myocardiopathy.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9121,"journal":{"name":"Birth Defects Research","volume":"116 11","pages":""},"PeriodicalIF":1.6,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142567049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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