Cited by 64

The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.

Influence of second-hand smoke and prenatal tobacco smoke exposure on biomarkers, genetics and physiological processes in children-an overview in research insights of the last few years

Braun, Markus, Klingelhöfer, Doris, Oremek, Gerhard M., Quarcoo, David, Groneberg, David A.·2020·International Journal of Environmental Research and Public Health

Abstract

Children are commonly exposed to second-hand smoke (SHS) in the domestic environment or inside vehicles of smokers. Unfortunately, prenatal tobacco smoke (PTS) exposure is still common, too. SHS is hazardous to the health of smokers and non-smokers, but especially to that of children. SHS and PTS increase the risk for children to develop cancers and can trigger or worsen asthma and allergies, modulate the immune status, and is harmful to lung, heart and blood vessels. Smoking during pregnancy can cause pregnancy complications and poor birth outcomes as well as changes in the development of the foetus. Lately, some of the molecular and genetic mechanisms that cause adverse health effects in children have been identified. In this review, some of the current insights are discussed. In this regard, it has been found in children that SHS and PTS exposure is associated with changes in levels of enzymes, hormones, and expression of genes, micro RNAs, and proteins. PTS and SHS exposure are major elicitors of mechanisms of oxidative stress. Genetic predisposition can compound the health effects of PTS and SHS exposure. Epigenetic effects might influence in utero gene expression and disease susceptibility. Hence, the limitation of domestic and public exposure to SHS as well as PTS exposure has to be in the focus of policymakers and the public in order to save the health of children at an early age. Global substantial smoke-free policies, health communication campaigns, and behavioural interventions are useful and should be mandatory.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.3390/ijerph17093212

Cites

11 of 11 references verified0 citation errors · 0 not checkable

Statistics

Figures

Figure 1 Adverse health effects in children induced by second-hand smoke and prenatal tobacco smoke exposure. COPD = chronic obstructive pulmonary disease.
Figure 1 Adverse health effects in children induced by second-hand smoke and prenatal tobacco smoke exposure. COPD = chronic obstructive pulmonary disease.CC BY · PubMed Central

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Show all 11 references

Research works printed but not linked: 174

  1. Protano, 2011, The new danger of thirdhand smoke: Why passive smoking does not stop at secondhand smoke, Environ. Health Perspect., 119, A422, 10.1289/ehp.1103956 · DOI
  2. Tsai, 2018, Exposure to Secondhand Smoke Among Nonsmokers - United States, 1988–2014, MMWR Morb. Mortal. Wkly. Rep., 67, 1342, 10.15585/mmwr.mm6748a3 · DOI
  3. Besaratinia, 2008, Second-hand smoke and human lung cancer, Lancet Oncol., 9, 657, 10.1016/S1470-2045(08)70172-4 · DOI
  4. Lee, 2016, Environmental tobacco smoke exposure and risk of breast cancer in nonsmoking women. An updated review and meta-analysis, Inhal. Toxicol., 28, 431, 10.1080/08958378.2016.1210701 · DOI
  5. Farber, 2015, Protecting Children From Tobacco, Nicotine, and Tobacco Smoke, Pediatrics, 136, e1439, 10.1542/peds.2015-3110 · DOI
  6. DiGiacomo, S.I., Jazayeri, M.A., Barua, R.S., and Ambrose, J.A. (2018). Environmental Tobacco Smoke and Cardiovascular Disease. Int. J. Environ. Res. Public Health, 16. · DOI
  7. Strzelak, A., Ratajczak, A., Adamiec, A., and Feleszko, W. (2018). Tobacco Smoke Induces and Alters Immune Responses in the Lung Triggering Inflammation, Allergy, Asthma and Other Lung Diseases: A Mechanistic Review. Int. J. Environ. Res. Public Health, 15. · DOI
  8. Rahman, 1999, Lung glutathione and oxidative stress: Implications in cigarette smoke-induced airway disease, Am. J. Physiol., 277, L1067
  9. Mund, 2013, Smoking and pregnancy—A review on the first major environmental risk factor of the unborn, Int. J. Environ. Res. Public Health, 10, 6485, 10.3390/ijerph10126485 · DOI
  10. Waterland, 2007, Epigenetic epidemiology of the developmental origins hypothesis, Annu. Rev. Nutr., 27, 363, 10.1146/annurev.nutr.27.061406.093705 · DOI
  11. U.S. Department of Health and Human Services (2019, September 17). The Health Consequences of Smoking—50 Years of Progress; A Report of the Surgeon General, Available online: https://www.ncbi.nlm.nih.gov/books/NBK179276/pdf/Bookshelf_NBK179276.pdf.
  12. Maier, 2002, Lung function of school children with low levels of alpha1-antitrypsin and tobacco smoke exposure, Eur. Respir. J., 19, 1099, 10.1183/09031936.02.00104302 · DOI
  13. Chen, 2016, Environmental Exposure and Genetic Predisposition as Risk Factors for Asthma in China, Allergy Asthma Immunol. Res., 8, 92, 10.4168/aair.2016.8.2.92 · DOI
  14. Homa, 2015, Vital signs: Disparities in nonsmokers’ exposure to secondhand smoke--United States, 1999–2012, MMWR Morb. Mortal. Wkly. Rep., 64, 103
  15. Lupsa, 2015, Urinary cotinine levels and environmental tobacco smoke in mothers and children of Romania, Portugal and Poland within the European human biomonitoring pilot study, Environ. Res., 141, 106, 10.1016/j.envres.2015.03.018 · DOI
  16. Lau, 2014, Protecting our children from environmental tobacco smoke: One of our great healthcare challenges, Eur. Heart J., 35, 2452, 10.1093/eurheartj/ehu098 · DOI
  17. Dubois, 2002, Biochemistry and molecular biology of gelatinase B or matrix metalloproteinase-9 (MMP-9), Crit. Rev. Biochem. Mol., 37, 375, 10.1080/10409230290771546 · DOI
  18. De, 2011, The effect of passive smoking on the levels of matrix metalloproteinase 9 in nasal secretions of children, Am. J. Rhinol. Allergy, 25, 226, 10.2500/ajra.2011.25.3623 · DOI
  19. Vignola, 1998, Sputum metalloproteinase-9/tissue inhibitor of metalloproteinase-1 ratio correlates with airflow obstruction in asthma and chronic bronchitis, Am. J. Respir. Crit. Care Med., 158, 1945, 10.1164/ajrccm.158.6.9803014 · DOI
  20. Kopp, 2019, Secondhand smoke alters arachidonic acid metabolism and inflammation in infants and children with cystic fibrosis, Thorax, 74, 237, 10.1136/thoraxjnl-2018-211845 · DOI
  21. Yilmaz, 2018, Secondhand tobacco smoke and severity in wheezing children: Nasal oxidant stress and inflammation, J. Asthma, 55, 477, 10.1080/02770903.2017.1350970 · DOI
  22. Lambrecht, 2019, The Cytokines of Asthma, Immunity, 50, 975, 10.1016/j.immuni.2019.03.018 · DOI
  23. Berry, 2007, TNF-alpha in asthma, Curr. Opin. Pharmacol., 7, 279, 10.1016/j.coph.2007.03.001 · DOI
  24. Chahal, 2017, Maternal Smoking and Newborn Cytokine and Immunoglobulin Levels, Nicotine Tob. Res., 19, 789
  25. Wilson, 2012, Secondhand smoke exposure and serum cytokine levels in healthy children, Cytokine, 60, 34, 10.1016/j.cyto.2012.06.236 · DOI
  26. Mahabee-Gittens, E.M., Merianos, A.L., Fulkerson, P.C., Stone, L., and Matt, G.E. (2019). The Association of Environmental Tobacco Smoke Exposure and Inflammatory Markers in Hospitalized Children. Int. J. Environ. Res. Public Health, 16. · DOI
  27. Riis, 2015, Salivary cytokines as a minimally-invasive measure of immune functioning in young children: Correlates of individual differences and sensitivity to laboratory stress, Dev. Psychobiol., 57, 153, 10.1002/dev.21271 · DOI
  28. Feleszko, 2006, Parental tobacco smoking is associated with augmented IL-13 secretion in children with allergic asthma, J. Allergy Clin. Immunol., 117, 97, 10.1016/j.jaci.2005.09.008 · DOI
  29. Laitinen, 1993, Leukotriene E4 and granulocytic infiltration into asthmatic airways, Lancet, 341, 989, 10.1016/0140-6736(93)91073-U · DOI
  30. Kumlin, 2000, Measurement of leukotrienes in humans, Am. J. Respir. Crit. Care Med., 161, S102, 10.1164/ajrccm.161.supplement_1.ltta-20 · DOI
  31. Lazarus, 2007, Smoking affects response to inhaled corticosteroids or leukotriene receptor antagonists in asthma, Am. J. Respir. Crit. Care Med., 175, 783, 10.1164/rccm.200511-1746OC · DOI
  32. Rabinovitch, 2008, Exposure to tobacco smoke increases leukotriene E4-related albuterol usage and response to montelukast, J. Allergy Clin. Immunol., 121, 1365, 10.1016/j.jaci.2008.03.016 · DOI
  33. Rabinovitch, 2011, Urinary leukotriene E(4) levels identify children with tobacco smoke exposure at risk for asthma exacerbation, J. Allergy Clin. Immunol., 128, 323, 10.1016/j.jaci.2011.05.035 · DOI
  34. Kott, 2008, Effect of secondhand cigarette smoke, RSV bronchiolitis and parental asthma on urinary cysteinyl LTE4, Pediatr. Pulmonol., 43, 760, 10.1002/ppul.20853 · DOI
  35. Chilmonczyk, 1993, Association between exposure to environmental tobacco smoke and exacerbations of asthma in children, N. Engl. J. Med., 328, 1665, 10.1056/NEJM199306103282303 · DOI
  36. Lang, 2013, Biologic mechanisms of environmental tobacco smoke in children with poorly controlled asthma: Results from a multicenter clinical trial, J. Allergy Clin. Immunol. Pract., 1, 172, 10.1016/j.jaip.2012.11.006 · DOI
  37. Furuya, 2013, Passive smoking induces leukotriene production in children: Influence of asthma, J. Asthma, 50, 347, 10.3109/02770903.2013.773009 · DOI
  38. Gill, 2014, Low-level environmental tobacco smoke exposure and inflammatory biomarkers in children with asthma, J. Asthma, 51, 355, 10.3109/02770903.2013.823446 · DOI
  39. Marmarinos, 2015, Urinary leukotriene E4 levels in atopic and non-atopic preschool children with recurrent episodic (viral) wheezing: A potential marker?, J. Asthma, 52, 554, 10.3109/02770903.2014.990092 · DOI
  40. Chiu, C.Y., Tsai, M.H., Yao, T.C., Tu, Y.L., Hua, M.C., Yeh, K.W., and Huang, J.L. (2014). Urinary LTE4 levels as a diagnostic marker for IgE-mediated asthma in preschool children: A birth cohort study. PLoS ONE, 9. · DOI
  41. Hagan, 2017, Urinary Leukotriene E4 to Determine Aspirin Intolerance in Asthma: A Systematic Review and Meta-Analysis, J. Allergy Clin. Immunol. Pract., 5, 990, 10.1016/j.jaip.2016.11.004 · DOI
  42. Hoffman, 2018, Urinary Leukotriene E4 as a Biomarker of Exposure, Susceptibility, and Risk in Asthma: An Update, Immunol. Allergy Clin., 38, 599
  43. Taal, 2011, Maternal smoking during pregnancy and kidney volume in the offspring: The Generation R Study, Pediatr. Nephrol., 26, 1275, 10.1007/s00467-011-1848-3 · DOI
  44. Hogan, 2007, Association of cigarette smoking with albuminuria in the United States: The third National Health and Nutrition Examination Survey, Ren. Fail., 29, 133, 10.1080/08860220601098888 · DOI
  45. Omoloja, 2011, Cigarette smoking and second-hand smoking exposure in adolescents with chronic kidney disease: A study from the Midwest Pediatric Nephrology Consortium, Nephrol. Dial. Transplant., 26, 908, 10.1093/ndt/gfq475 · DOI
  46. Loeffler, 2013, Kidney function and tobacco smoke exposure in US adolescents, Pediatrics, 131, e1415, 10.1542/peds.2012-3201 · DOI
  47. Omoloja, 2013, Secondhand smoke exposure is associated with proteinuria in children with chronic kidney disease, Pediatr. Nephrol., 28, 1243, 10.1007/s00467-013-2456-1 · DOI
  48. Kooijman, 2015, Fetal Smoke Exposure and Kidney Outcomes in School-Aged Children, Am. J. Kidney Dis., 66, 412, 10.1053/j.ajkd.2014.12.008 · DOI
  49. Torok, 2000, Passive smoking impairs endothelium-dependent relaxation of isolated rabbit arteries, Physiol. Res., 49, 135
  50. Hackshaw, 2011, Maternal smoking in pregnancy and birth defects: A systematic review based on 173 687 malformed cases and 11.7 million controls, Hum. Reprod. Update, 17, 589, 10.1093/humupd/dmr022 · DOI
  51. Groner, 2015, Secondhand smoke exposure and endothelial stress in children and adolescents, Acad. Pediatr., 15, 54, 10.1016/j.acap.2014.09.003 · DOI
  52. Raitakari, 2003, Cardiovascular risk factors in childhood and carotid artery intima-media thickness in adulthood: The Cardiovascular Risk in Young Finns Study, JAMA, 290, 2277, 10.1001/jama.290.17.2277 · DOI · Paper page
  53. Gunes, 2007, Influence of maternal smoking on neonatal aortic intima-media thickness, serum IGF-I and IGFBP-3 levels, Eur. J. Pediatr., 166, 1039, 10.1007/s00431-006-0376-9 · DOI
  54. Geerts, 2012, Parental smoking and vascular damage in their 5-year-old children, Pediatrics, 129, 45, 10.1542/peds.2011-0249 · DOI
  55. Gall, 2014, Exposure to parental smoking in childhood or adolescence is associated with increased carotid intima-media thickness in young adults: Evidence from the Cardiovascular Risk in Young Finns study and the Childhood Determinants of Adult Health Study, Eur. Heart J., 35, 2484, 10.1093/eurheartj/ehu049 · DOI
  56. Groh, 2019, Childhood Tobacco Smoke Exposure and Risk of Atrial Fibrillation in Adulthood, J. Am. Coll. Cardiol., 74, 1658, 10.1016/j.jacc.2019.07.060 · DOI
  57. Black, 2004, C-reactive Protein, J. Biol. Chem., 279, 48487, 10.1074/jbc.R400025200 · DOI · Paper page
  58. Wilkinson, 2007, Secondhand smoke exposure and C-reactive protein levels in youth, Nicotine Tob. Res., 9, 305, 10.1080/14622200601080299 · DOI
  59. Nagel, 2009, Environmental tobacco smoke and cardiometabolic risk in young children: Results from a survey in south-west Germany, Eur. Heart J., 30, 1885, 10.1093/eurheartj/ehp180 · DOI
  60. Kang, E., Kim, S.Y., Chang, S.S., Lim, S., Kim, H.C., Lee, C.G., Kim, Y.M., Kim, S.Y., Lee, K.J., and Kim, S. (2017). Environmental Tobacco Smoke Exposure at Home and High-Sensitivity C-Reactive Protein Levels in Three-to-Five-Year-Old Children. Int. J. Environ. Res. Public Health, 14. · DOI
  61. Wang, 2017, Exposure to Parental Smoking in Childhood is Associated with High C-Reactive Protein in Adulthood: The Cardiovascular Risk in Young Finns Study, J. Atheroscler. Thromb., 24, 1231, 10.5551/jat.40568 · DOI
  62. Palomares, 2010, Role of Treg in immune regulation of allergic diseases, Eur. J. Immunol., 40, 1232, 10.1002/eji.200940045 · DOI
  63. Hinz, 2012, Cord blood Tregs with stable FOXP3 expression are influenced by prenatal environment and associated with atopic dermatitis at the age of one year, Allergy, 67, 380, 10.1111/j.1398-9995.2011.02767.x · DOI · Paper page
  64. Herberth, 2014, Maternal and cord blood miR-223 expression associates with prenatal tobacco smoke exposure and low regulatory T-cell numbers, J. Allergy Clin. Immunol., 133, 543, 10.1016/j.jaci.2013.06.036 · DOI
  65. Hedrick, 2012, FOXO transcription factors throughout T cell biology, Nat. Rev. Immunol., 12, 649, 10.1038/nri3278 · DOI · Paper page
  66. Lee, 2018, Increased miR-223 expression in foetal organs is a signature of acute chorioamnionitis with systemic consequences, J. Cell. Mol. Med., 22, 1179, 10.1111/jcmm.13377 · DOI
  67. Jing, 2019, Passive smoking induces pediatric asthma by affecting the balance of Treg/Th17 cells, Pediatr. Res., 85, 469, 10.1038/s41390-019-0276-0 · DOI
  68. Shi, 2011, Coexistence of Th1/Th2 and Th17/Treg imbalances in patients with allergic asthma, Chin. Med. J., 124, 1951
  69. Vardavas, 2010, Passive smoking alters circulating naive/memory lymphocyte T-cell subpopulations in children, Pediatr. Allergy Immunol., 21, 1171, 10.1111/j.1399-3038.2010.01039.x · DOI
  70. Marseglia, 2009, Passive exposure to smoke results in defective interferon-gamma production by adenoids in children with recurrent respiratory infections, J. Interferon Cytokine Res., 29, 427, 10.1089/jir.2008.0108 · DOI
  71. Tagliacarne, 2015, Impact of passive smoke and/or atopy on adenoid immunoglobulin production in children, Immunol. Lett., 165, 70, 10.1016/j.imlet.2015.04.002 · DOI
  72. Yao, 2016, Tobacco smoke exposure and multiplexed immunoglobulin E sensitization in children: A population-based study, Allergy, 71, 90, 10.1111/all.12775 · DOI
  73. Thacher, 2016, Parental smoking and development of allergic sensitization from birth to adolescence, Allergy, 71, 239, 10.1111/all.12792 · DOI
  74. Feleszko, 2014, Environmental tobacco smoke exposure and risk of allergic sensitisation in children: A systematic review and meta-analysis, Arch. Dis. Child., 99, 985, 10.1136/archdischild-2013-305444 · DOI
  75. Hirata, 2010, Passive smoking is associated with lower serum HDL-C levels in school children, Pediatr. Int., 52, 252, 10.1111/j.1442-200X.2009.02957.x · DOI
  76. Hamdy, 2011, Effect of passive smoking on blood lymphocyte apoptosis in children, Eur. J. Clin. Investig., 41, 387, 10.1111/j.1365-2362.2010.02420.x · DOI
  77. Xie, 2010, Environmental tobacco use and indicators of metabolic syndrome in Chinese adults, Nicotine Tob. Res., 12, 198, 10.1093/ntr/ntp194 · DOI
  78. Groner, 2017, Secondhand Smoke Exposure and Preclinical Markers of Cardiovascular Risk in Toddlers, J. Pediatr., 189, 155, 10.1016/j.jpeds.2017.06.032 · DOI
  79. Ayer, 2011, Maternal cigarette smoking is associated with reduced high-density lipoprotein cholesterol in healthy 8-year-old children, Eur. Heart J., 32, 2446, 10.1093/eurheartj/ehr174 · DOI
  80. Beilin, 2013, Gender difference in the relationship between passive smoking exposure and HDL-cholesterol levels in late adolescence, J. Clin. Endocrinol. Metab., 98, 2126, 10.1210/jc.2013-1016 · DOI
  81. Kallio, 2010, Arterial intima-media thickness, endothelial function, and apolipoproteins in adolescents frequently exposed to tobacco smoke, Circ. Cardiovasc. Qual. Outcomes, 3, 196, 10.1161/CIRCOUTCOMES.109.857771 · DOI
  82. Skjaerven, 2012, Exposure to tobacco smoke in utero and subsequent plasma lipids, ApoB, and CRP among adult women in the MoBa cohort, Environ. Health Perspect., 120, 1532, 10.1289/ehp.1104563 · DOI
  83. Krumsiek, 2016, Metabolomics reveals effects of maternal smoking on endogenous metabolites from lipid metabolism in cord blood of newborns, Metabolomics, 12, 76, 10.1007/s11306-016-0983-z · DOI
  84. Zakhar, 2016, Passive and Active Tobacco Exposure and Children’s Lipid Profiles, Nicotine Tob. Res., 18, 982, 10.1093/ntr/ntv158 · DOI
  85. Schieber, 2014, ROS function in redox signaling and oxidative stress, Curr. Biol., 24, R453, 10.1016/j.cub.2014.03.034 · DOI · Paper page
  86. Halliwell, 1994, Free radicals, antioxidants, and human disease: Curiosity, cause, or consequence?, Lancet, 344, 721, 10.1016/S0140-6736(94)92211-X · DOI
  87. Sahiner, 2018, Oxidative stress in asthma: Part of the puzzle, Pediatr. Allergy Immunol., 29, 789, 10.1111/pai.12965 · DOI
  88. Raghuveer, 2016, Cardiovascular Consequences of Childhood Secondhand Tobacco Smoke Exposure: Prevailing Evidence, Burden, and Racial and Socioeconomic Disparities: A Scientific Statement From the American Heart Association, Circulation, 134, e336, 10.1161/CIR.0000000000000443 · DOI
  89. Perrone, 2012, Biomarkers of oxidative stress in fetal and neonatal diseases, J. Matern. Fetal Neonatal Med., 25, 2575, 10.3109/14767058.2012.718004 · DOI
  90. Bono, 2014, Oxidative stress in adolescent passive smokers living in urban and rural environments, Int. J. Hyg. Environ. Health, 217, 287, 10.1016/j.ijheh.2013.06.008 · DOI
  91. Squillacioti, G., Bellisario, V., Grignani, E., Mengozzi, G., Bardaglio, G., Dalmasso, P., and Bono, R. (2019). The Asti Study: The Induction of Oxidative Stress in A Population of Children According to Their Body Composition and Passive Tobacco Smoking Exposure. Int. J. Environ. Res. Public Health, 16. · DOI
  92. Li, 2014, Oxidative stress, redox signalling and endothelial dysfunction in ageing-related neurodegenerative diseases: A role of NADPH oxidase 2, Br. J. Clin. Pharmacol., 78, 441, 10.1111/bcp.12357 · DOI
  93. Loffredo, 2018, Role of NADPH oxidase-2 and oxidative stress in children exposed to passive smoking, Thorax, 73, 986, 10.1136/thoraxjnl-2017-211293 · DOI
  94. Roberts, 2009, Oxidative stress and metabolic syndrome, Life Sci., 84, 705, 10.1016/j.lfs.2009.02.026 · DOI
  95. Weitzman, 2005, Tobacco smoke exposure is associated with the metabolic syndrome in adolescents, Circulation, 112, 862, 10.1161/CIRCULATIONAHA.104.520650 · DOI
  96. Moore, 2016, Interactions Between Diet and Exposure to Secondhand Smoke on Metabolic Syndrome Among Children: NHANES 2007–2010, J. Clin. Endocrinol. Metab., 101, 52, 10.1210/jc.2015-2477 · DOI
  97. Chelchowska, 2016, Cord Blood Adiponectin and Visfatin Concentrations in relation to Oxidative Stress Markers in Neonates Exposed and Nonexposed In Utero to Tobacco Smoke, Oxid. Med. Cell. Longev., 2016, 4569108, 10.1155/2016/4569108 · DOI
  98. Bono, 2015, Urban air and tobacco smoke as conditions that increase the risk of oxidative stress and respiratory response in youth, Environ. Res., 137, 141, 10.1016/j.envres.2014.12.008 · DOI
  99. Kobayashi, 2014, Passive smoking impairs histone deacetylase-2 in children with severe asthma, Chest, 145, 305, 10.1378/chest.13-0835 · DOI
  100. Rathkopf, 2014, Passive smoking impairs histone deacetylase-2 in children with severe asthma, Pediatrics, 134, S147, 10.1542/peds.2014-1817Z · DOI
  101. Podlecka, 2018, Secondhand smoke exposure increased the need for inhaled corticosteroids in children with asthma, Ann. Allergy Asthma Immunol., 121, 119, 10.1016/j.anai.2018.04.021 · DOI
  102. Lisboa, 2012, Obesity and endocrine dysfunction programmed by maternal smoking in pregnancy and lactation, Front. Physiol., 3, 437, 10.3389/fphys.2012.00437 · DOI
  103. Paslakis, 2014, Intrauterine exposure to cigarette smoke is associated with increased ghrelin concentrations in adulthood, Neuroendocrinology, 99, 123, 10.1159/000363325 · DOI
  104. Duskova, 2014, The effects of smoking on steroid metabolism and fetal programming, J. Steroid Biochem. Mol. Biol., 139, 138, 10.1016/j.jsbmb.2013.05.003 · DOI
  105. Gollenberg, 2015, In utero exposure to cigarette smoking, environmental tobacco smoke and reproductive hormones in US girls approaching puberty, Horm. Res. Paediatr., 83, 36, 10.1159/000369168 · DOI
  106. Ernst, 2012, Maternal smoking during pregnancy and reproductive health of daughters: A follow-up study spanning two decades, Hum. Reprod., 27, 3593, 10.1093/humrep/des337 · DOI
  107. Ittermann, 2013, Relationship of smoking and/or passive exposure to tobacco smoke on the association between serum thyrotropin and body mass index in large groups of adolescents and children, Thyroid, 23, 262, 10.1089/thy.2012.0110 · DOI
  108. Filis, P., Hombach-Klonisch, S., Ayotte, P., Nagrath, N., Soffientini, U., Klonisch, T., O’Shaughnessy, P., and Fowler, P.A. (2018). Maternal smoking and high BMI disrupt thyroid gland development. BMC Med., 16. · DOI
  109. Singhal, 2002, Influence of leptin on arterial distensibility: A novel link between obesity and cardiovascular disease?, Circulation, 106, 1919, 10.1161/01.CIR.0000033219.24717.52 · DOI
  110. Wilce, 1994, Structure and function of glutathione S-transferases, Biochim. Biophys. Acta, 1205, 1, 10.1016/0167-4838(94)90086-8 · DOI
  111. Panasevich, 2010, Interaction between early maternal smoking and variants in TNF and GSTP1 in childhood wheezing, Clin. Exp. Allergy, 40, 458, 10.1111/j.1365-2222.2010.03452.x · DOI
  112. Lee, 2007, Associations of glutathione S-transferase P1, M1, and environmental tobacco smoke with wheezing illness in school children, Allergy, 62, 641, 10.1111/j.1398-9995.2007.01380.x · DOI
  113. Palmer, 2006, Glutathione S-transferase M1 and P1 genotype, passive smoking, and peak expiratory flow in asthma, Pediatrics, 118, 710, 10.1542/peds.2005-3030 · DOI
  114. Wu, 2014, Gender-dependent effect of GSTM1 genotype on childhood asthma associated with prenatal tobacco smoke exposure, Biomed. Res. Int., 2014, 769452, 10.1155/2014/769452 · DOI
  115. Lee, S.Y., Kim, B.S., Kwon, S.O., Oh, S.Y., Shin, H.L., Jung, Y.H., Lee, E., Yang, S.I., Kim, H.Y., and Seo, J.H. (2015). Modification of additive effect between vitamins and ETS on childhood asthma risk according to GSTP1 polymorphism: A cross-sectional study. BMC Pulm. Med., 15. · DOI
  116. Wenten, 2009, In utero smoke exposure, glutathione S-transferase P1 haplotypes, and respiratory illness-related absence among schoolchildren, Pediatrics, 123, 1344, 10.1542/peds.2008-1892 · DOI
  117. Turner, 2018, Variants in genes coding for glutathione S-transferases and asthma outcomes in children, Pharmacogenomics, 19, 707, 10.2217/pgs-2018-0027 · DOI
  118. Morales, 2009, GSTM1 polymorphisms modify the effect of maternal smoking during pregnancy on cognitive functioning in preschoolers, Int. J. Epidemiol., 38, 690, 10.1093/ije/dyp141 · DOI
  119. Filonzi, 2018, Detoxification genes polymorphisms in SIDS exposed to tobacco smoke, Gene, 648, 1, 10.1016/j.gene.2018.01.034 · DOI
  120. Wang, 2010, GSTM1, GSTP1, prenatal smoke exposure, and atopic dermatitis, Ann. Allerg Asthma Immunol., 105, 124, 10.1016/j.anai.2010.04.017 · DOI
  121. Li, 2015, Modification of the association between maternal smoke exposure and congenital heart defects by polymorphisms in glutathione S-transferase genes, Sci. Rep., 5, 14915, 10.1038/srep14915 · DOI
  122. Dai, 2019, Interaction of Glutathione S-Transferase M1, T1, and P1 Genes With Early Life Tobacco Smoke Exposure on Lung Function in Adolescents, Chest, 155, 94, 10.1016/j.chest.2018.08.1079 · DOI
  123. Wenten, 2005, TNF-308 modifies the effect of second-hand smoke on respiratory illness-related school absences, Am. J. Respir. Crit. Care Med., 172, 1563, 10.1164/rccm.200503-490OC · DOI
  124. Salam, 2007, Transforming growth factor- 1 C-509T polymorphism, oxidant stress, and early-onset childhood asthma, Am. J. Respir. Crit. Care Med., 176, 1192, 10.1164/rccm.200704-561OC · DOI
  125. Smith, 2008, Environmental tobacco smoke and interleukin 4 polymorphism (C-589T) gene: Environment interaction increases risk of wheezing in African-American infants, J. Pediatr., 152, 709, 10.1016/j.jpeds.2007.10.011 · DOI
  126. Sadeghnejad, 2008, IL13 gene polymorphisms modify the effect of exposure to tobacco smoke on persistent wheeze and asthma in childhood, a longitudinal study, Respir. Res., 9, 2, 10.1186/1465-9921-9-2 · DOI
  127. Wright, 1990, CD14, a receptor for complexes of lipopolysaccharide (LPS) and LPS binding protein, Science, 249, 1431, 10.1126/science.1698311 · DOI
  128. Bottema, 2008, Interleukin 13, CD14, pet and tobacco smoke influence atopy in three Dutch cohorts: The allergenic study, Eur. Respir. J., 32, 593, 10.1183/09031936.00162407 · DOI
  129. Hussein, 2013, CD14 tobacco gene-environment interaction in atopic children, Cell. Immunol., 285, 31, 10.1016/j.cellimm.2013.08.001 · DOI
  130. Bouzigon, 2008, Effect of 17q21 variants and smoking exposure in early-onset asthma, N. Engl. J. Med., 359, 1985, 10.1056/NEJMoa0806604 · DOI
  131. Flory, 2009, 17q12-21 variants interact with smoke exposure as a risk factor for pediatric asthma but are equally associated with early-onset versus late-onset asthma in North Americans of European ancestry, J. Allergy Clin. Immunol., 124, 605, 10.1016/j.jaci.2009.05.047 · DOI
  132. Duijts, 2012, Interaction of a 17q12 variant with both fetal and infant smoke exposure in the development of childhood asthma-like symptoms, Allergy, 67, 767, 10.1111/j.1398-9995.2012.02819.x · DOI
  133. Strachan, 2015, 17q21 gene variation is not associated with asthma in adulthood, Allergy, 70, 107, 10.1111/all.12537 · DOI
  134. Morita, 2009, Smoking exposure, 17q21 variants, and early-onset asthma, N. Engl. J. Med., 360, 1255, 10.1056/NEJMc082444 · DOI
  135. Dizier, 2007, Evidence for gene x smoking exposure interactions in a genome-wide linkage screen of asthma and bronchial hyper-responsiveness in EGEA families, Eur. J. Hum. Genet., 15, 810, 10.1038/sj.ejhg.5201830 · DOI
  136. Dizier, 2016, Interaction between the DNAH9 gene and early smoke exposure in bronchial hyperresponsiveness, Eur. Respir. J., 47, 1072, 10.1183/13993003.00849-2015 · DOI
  137. Dizier, 2019, Interactive effect between ATPase-related genes and early-life tobacco smoke exposure on bronchial hyper-responsiveness detected in asthma-ascertained families, Thorax, 74, 254, 10.1136/thoraxjnl-2018-211797 · DOI
  138. Yang, 2009, Childhood exposure to secondhand smoke and functional mannose binding lectin polymorphisms are associated with increased lung cancer risk, Cancer Epidemiol. Prev. Biomark., 18, 3375, 10.1158/1055-9965.EPI-09-0986 · DOI
  139. Poetsch, 2010, A common FMO3 polymorphism may amplify the effect of nicotine exposure in sudden infant death syndrome (SIDS), Int. J. Legal. Med., 124, 301, 10.1007/s00414-010-0428-6 · DOI
  140. Boneva, 2001, Mortality associated with congenital heart defects in the United States: Trends and racial disparities, 1979–1997, Circulation, 103, 2376, 10.1161/01.CIR.103.19.2376 · DOI
  141. Tang, 2015, Genetic variation affects congenital heart defect susceptibility in offspring exposed to maternal tobacco use, Birth Defects Res. Part A Clin. Mol. Teratol., 103, 834, 10.1002/bdra.23370 · DOI
  142. Satokata, 1994, Msx1 deficient mice exhibit cleft palate and abnormalities of craniofacial and tooth development, Nat. Genet., 6, 348, 10.1038/ng0494-348 · DOI
  143. Krapels, 2008, The MSX1 allele 4 homozygous child exposed to smoking at periconception is most sensitive in developing nonsyndromic orofacial clefts, Hum. Genet., 124, 525, 10.1007/s00439-008-0569-6 · DOI
  144. NCBI (2020, February 21). National Center for Biotechnology Information, U.S. National Library of Medicine, Gene, Available online: https://www.ncbi.nlm.nih.gov/gene/.
  145. Monteiro, 2011, Maternal smoking and fetal sex significantly affect metabolic enzyme expression in the human fetal liver, J. Clin. Endocrinol. Metab., 96, 2851, 10.1210/jc.2011-1437 · DOI
  146. Drake, A.J., O’Shaughnessy, P.J., Bhattacharya, S., Monteiro, A., Kerrigan, D., Goetz, S., Raab, A., Rhind, S.M., Sinclair, K.D., and Meharg, A.A. (2015). In utero exposure to cigarette chemicals induces sex-specific disruption of one-carbon metabolism and DNA methylation in the human fetal liver. BMC Med., 13. · DOI
  147. Filis, 2015, Maternal Smoking Dysregulates Protein Expression in Second Trimester Human Fetal Livers in a Sex-Specific Manner, J. Clin. Endocrinol. Metab., 100, E861, 10.1210/jc.2014-3941 · DOI
  148. Du, 2007, Beginning to understand microRNA function, Cell Res., 17, 661, 10.1038/cr.2007.67 · DOI
  149. Maccani, 2010, Maternal cigarette smoking during pregnancy is associated with downregulation of miR-16, miR-21, and miR-146a in the placenta, Epigenetics, 5, 583, 10.4161/epi.5.7.12762 · DOI · Paper page
  150. Gao, 2018, Self-reported prenatal tobacco smoke exposure, AXL gene-body methylation, and childhood asthma phenotypes, Clin. Epigenet., 10, 98, 10.1186/s13148-018-0532-x · DOI
  151. Mudduluru, 2011, Regulation of Axl receptor tyrosine kinase expression by miR-34a and miR-199a/b in solid cancer, Oncogene, 30, 2888, 10.1038/onc.2011.13 · DOI
  152. Liu, 2019, Indoor air pollution aggravates asthma in Chinese children and induces the changes in serum level of miR-155, Int. J. Environ. Health Res., 29, 22, 10.1080/09603123.2018.1506569 · DOI
  153. Jylhava, 2017, Biological Age Predictors, EBioMedicine, 21, 29, 10.1016/j.ebiom.2017.03.046 · DOI · Paper page
  154. Clemente, 2020, Early life tobacco exposure and children’s telomere length: The HELIX project, Sci. Total Environ., 711, 135028, 10.1016/j.scitotenv.2019.135028 · DOI
  155. Martino, 2011, Epigenetics and prenatal influences on asthma and allergic airways disease, Chest, 139, 640, 10.1378/chest.10-1800 · DOI
  156. Ganu, 2012, Early origins of adult disease: Approaches for investigating the programmable epigenome in humans, nonhuman primates, and rodents, ILAR J., 53, 306, 10.1093/ilar.53.3-4.306 · DOI
  157. Wadhwa, 2009, Developmental origins of health and disease: Brief history of the approach and current focus on epigenetic mechanisms, Semin. Reprod. Med., 27, 358, 10.1055/s-0029-1237424 · DOI
  158. Nielsen, 2016, DNA methylation alterations in response to prenatal exposure of maternal cigarette smoking: A persistent epigenetic impact on health from maternal lifestyle?, Arch. Toxicol., 90, 231, 10.1007/s00204-014-1426-0 · DOI
  159. Breton, 2009, Prenatal tobacco smoke exposure affects global and gene-specific DNA methylation, Am. J. Respir. Crit. Care Med., 180, 462, 10.1164/rccm.200901-0135OC · DOI
  160. Suter, 2010, In utero tobacco exposure epigenetically modifies placental CYP1A1 expression, Metabolism, 59, 1481, 10.1016/j.metabol.2010.01.013 · DOI · Paper page
  161. Suter, 2011, Maternal tobacco use modestly alters correlated epigenome-wide placental DNA methylation and gene expression, Epigenetics, 6, 1284, 10.4161/epi.6.11.17819 · DOI · Paper page
  162. Murphy, 2012, Gender-specific methylation differences in relation to prenatal exposure to cigarette smoke, Gene, 494, 36, 10.1016/j.gene.2011.11.062 · DOI
  163. Wang, 2013, Prenatal smoke exposure, DNA methylation, and childhood atopic dermatitis, Clin. Exp. Allergy, 43, 535, 10.1111/cea.12108 · DOI
  164. Joubert, 2012, 450K epigenome-wide scan identifies differential DNA methylation in newborns related to maternal smoking during pregnancy, Environ. Health Perspect., 120, 1425, 10.1289/ehp.1205412 · DOI · Paper page
  165. Markunas, 2014, Identification of DNA methylation changes in newborns related to maternal smoking during pregnancy, Environ. Health Perspect., 122, 1147, 10.1289/ehp.1307892 · DOI
  166. Zakarya, 2019, Epigenetic impacts of maternal tobacco and e-vapour exposure on the offspring lung, Clin. Epigenet., 11, 32, 10.1186/s13148-019-0631-3 · DOI
  167. Den Dekker, H.T., Burrows, K., Felix, J.F., Salas, L.A., Nedeljkovic, I., Yao, J., Rifas-Shiman, S.L., Ruiz-Arenas, C., Amin, N., and Bustamante, M. (2019). Newborn DNA-methylation, childhood lung function, and the risks of asthma and COPD across the life course. Eur. Respir. J., 53. · DOI
  168. Runyon, R.S., Cachola, L.M., Rajeshuni, N., Hunter, T., Garcia, M., Ahn, R., Lurmann, F., Krasnow, R., Jack, L.M., and Miller, R.L. (2012). Asthma discordance in twins is linked to epigenetic modifications of T cells. PLoS ONE, 7. · DOI
  169. Reinius, L.E., Gref, A., Saaf, A., Acevedo, N., Joerink, M., Kupczyk, M., D’Amato, M., Bergstrom, A., Melen, E., and Scheynius, A. (2013). DNA methylation in the Neuropeptide S Receptor 1 (NPSR1) promoter in relation to asthma and environmental factors. PLoS ONE, 8. · DOI
  170. Haghighi, 2014, Opioid receptor mu 1 gene, fat intake and obesity in adolescence, Mol. Psychiatry, 19, 63, 10.1038/mp.2012.179 · DOI
  171. Lee, 2015, Prenatal exposure to cigarette smoke interacts with OPRM1 to modulate dietary preference for fat, J. Psychiatry Neurosci., 40, 38, 10.1503/jpn.130263 · DOI
  172. Oken, 2008, Maternal smoking during pregnancy and child overweight: Systematic review and meta-analysis, Int. J. Obes., 32, 201, 10.1038/sj.ijo.0803760 · DOI · Paper page
  173. Joas, 2012, Harmonised human biomonitoring in Europe: Activities towards an EU HBM framework, Int. J. Hyg. Environ. Health, 215, 172, 10.1016/j.ijheh.2011.08.010 · DOI
  174. Budnik, 2018, Diagnosis, monitoring and prevention of exposure-related non-communicable diseases in the living and working environment: DiMoPEx-project is designed to determine the impacts of environmental exposure on human health, J. Occup. Med. Toxicol., 13, 6, 10.1186/s12995-018-0186-9 · DOI

Metadata

Authors
Braun, M., Klingelhöfer, D., Oremek, G. M., Quarcoo, D., & Groneberg, D. A.
Affiliations
Institute of Occupational Medicine, Social Medicine and Environmental Medicine, Goethe University Frankfurt, D-60590 Frankfurt, Germany
Venue
International Journal of Environmental Research and Public Health
Publisher
MDPI AG
Published
2020-05-05
Volume
17
Issue
9
Pages
3212
ISSN
1660-4601
Cited by
64
References
11
Language
en

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review