Maternal smoking during pregnancy and offspring health outcomes: The role of epigenetic research in informing legal policy and practice

Hastings Law Journal

Volumn 64, Issue 6, 2013, Pages 1619-1648

  Smith, Taylor F ^a   Maccani, Matthew A ^b   Knopik, Valerie S ^a  

^a RHODE ISLAND HOSPITAL   (United States)

^b BROWN UNIVERSITY   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

EID: 84885204656     PISSN: 00178322     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Conference Paper

References (147)

1. See Tessa Roseboom et al., The Dutch Famine and its Long-Term Consequences for Adult Health, 82 EARLY HUM. DEV. 485, 486 (2006).
2. Epidemiological theory, such as the "developmental origins of health and disease" hypothesis, provides a framework for understanding the causes and patterns of disease. See generally Peter D. Gluckman & Mark A. Hanson, Living with the Past: Evolution, Development, and Patterns of Disease, 305 SCIENCE 1733 (2004).
3. Epigenetics researches changes in gene expression that are not caused by changes in the sequence of DNA. See generally Adrian Bird, Perceptions of Epigenetics, 447 NATURE 396 (2007).
4. See generally Benjamin G. Druss et al., The Most Expensive Medical Conditions In America, 21 HEALTH AFF., no. 4, 2002, at 105.
5. See Arialdi M. Minino & Betty L. Smith, Ctrs. for Disease Control & Prevention, 49 National Vital Statistics Reports 12, at 2-4 (Oct. 2001) (discussing the leading causes of death from 1999-2000, including diseases).
6. See generally Robert Barouki et al., Developmental Origins of Non-Communicable Disease: Implications for Research and Public Health, ENVIRONMENTAL HEALTH (Jun. 27, 2012, 11:42 AM), http://www.ehjoumal.net/content/ 11/1/42.
7. See generally Dawn P. Misra et al., Maternal Smoking and Birth Weight: Interaction with Parity and Mother's Own In Utero Exposure to Smoking, 16 EPIDEMIOLOGY 288 (2005).
8. See, e.g., D. J. P. Barker, The Origins of the Developmental Origins Theory, 261 J. INTERNAL MED. 412 (2007);
9. Pathik D. Wadhwa et al., Developmental Origins of Health and Disease: Brief History of the Approach and Current Focus on Epigenetic Mechanisms, 27 SEMINARS REPROD. MED. 358 (2009).
10. Roseboom et al., Effects of Prenatal Exposure to the Dutch Famine on Adult Disease in Later Life: An Overview, 185 MOLECULAR & CELLULAR ENDOCRINOLOGY 93 (2001).
11. See generally Gian-Paolo Ravelli et al., Obesity in Young Men After Famine Exposure In Utero and Early Infancy, 295 NEW ENG. J. MED. 349 (1976).
12. See generally E. S. Susser & S. P. Lin, Schizophrenia After Prenatal Exposure to the Dutch Hunger Winter of 1944-1945, 49 ARCHIVES GEN. PSYCHIATRY 983 (1992).
13. See, e.g., K. Latimer et al., Disruptive Behaviour Disorders: A Systematic Review of Environmental Antenatal and Early Years Risk Factors, 38 CHILD: CARE, HEALTH & DEV. 609, 611-28 (2012).
14. Valerie S. Knopik et al., The Epigenetics of Maternal Cigarette Smoking During Pregnancy and Effects on Child Development, 24 DEV. & PSYCHOPATHOLOGY 1377, 1379 (2012).
15. See generally C. N. Hales & D. J. P. Barker, Type 2 (Non-Insulin-Dependent) Diabetes Mellitus: the Thrifty Phenotype Hypothesis, 35 DIABETOLOGIA 595 (1992). According to Hales and Barker the "thrifty phenotype" describes the notion that fetal malnutrition is associated with restricted fetal growth and lasting changes in glucose-insulin metabolism which increases vulnerability for metabolic problems, including type 2 diabetes, when exposed to a nutrient rich postnatal environment.
16. see also David J. P. Barker & Phillipa M. Clark, Fetal Undemutrition and Disease in Later Life, 2 REVS. REFROD. 105, 109 (1997);
17. Susanne R. de Rooij et al., Prenatal Undemutrition and Cognitive Function in Late Adulthood, 107 PROCEEDINGS NAT'L ACAD. SCI. U. S. 16881, 16883 (2010).
18. Ahmet A. Baschat, Fetal Responses to Placental Insufficiency: An Update, 111 BJOG: INT'L J. OBSTETRICS & GYNAECOLOGY 1031, 1035 (2004).
19. Jing Fu & Per Olofsson, Restrained Cerebral Hyperperfusion in Response to Superimposed Acute Hypoxemia in Growth-Restricted Human Fetuses with Established Brain-Sparing Blood Flow, 82 EARLY HUM. DEV. 211, 215 (2006).
20. Sabine J. Roza et al., What Is Spared by Fetal Brain-Sparing? Fetal Circulatory Redistribution and Behavioral Problems in the General Population, 168 Am. J. EPIDEMIOLOGY 1145, 1145 (2008).
21. Ian C. G. Weaver et al., Epigenetic Programming by Maternal Behavior, 7 NATURE NEUROSCIENCE 847, 847 (2004).
22. Helen Sharp et al., Frequency of Infant Stroking Reported by Mothers Moderates the Effect of Prenatal Depression on Infant Behavioural and Physiological Outcomes, PLoS ONE, Oct. 2012, at 1, 8.
23. Peter D. Gluckman et al., Developmental Origins of Health and Disease: Reducing the Burden of Chronic Disease in the Next Generation, GENOME MED. (Feb. 24, 2010, 2:14 PM), http://www.genomemedicine.com/content/2/2/14.
24. Christina M. Hultman et al., Birth Weight and Attention-Deficit/ Hyperactivity Symptoms in Childhood and Early Adolescence: A Prospective Swedish Twin Study, 46 J. AM. ACAD. CHILD & ADOLESCENT PSYCHIATRY 370, 375 (2007).
25. D. O. Mook-Kanamori, Heritability Estimates of Body Size in Fetal Life and Early Childhood, PLoS ONE, July 2013, at 3-7.
26. See generally Valerie S. Knopik, Maternal Smoking During Pregnancy and Child Outcomes: Real or Spurious Effect?, 34 DEVELOPMENTAL NEUROPSYCHOLOGY 1 (2009).
27. See generally Kenneth S. Kendler & Jessica H. Baker, Genetic Influences on Measures of the Environment: A Systematic Review, 37 PSYCHOL. MED. 615 (2007).
28. Sara R. Jaffee & Thomas S. Price, The Implications of Genotype-Environment Correlation for Establishing Causal Processes in Psychopathology, 24 DEV. A PSYCHOPATHOLOGY 1253, 1253-54 (2012).
29. Terrie E. Moffitt et al., Strategy for Investigating Interactions Between Measured Genes and Measured Environments, 62 ARCHIVES GEN. PSYCHIATRY 473, 473 (2005).
30. 4 Genotyping at Murder Trials, 52 J. FORENSIC SCI. 1362, 1362 (2007).
31. See generally R. C. Bagot & M. J. Meaney, Epigenetics & the Biological Basis of Gene × Environment Interactions, 49 J. AM. ACAD. CHILD & ADOLESCENT PSYCHIATRY 752 (2010).
32. see Matthew A. Maccani & Carmen J. Marsit, Epigenetics in the Placenta, 62 AM. J. REPROD. IMMUNOLOGY 78, 78 (2009) ("There are only a few settings where the importance of this gene-environment interface is more profound than during intrauterine development, where the 'critical windows' are narrower and where disruption or modification can influence fetal development as well as lead to programming of health throughout the life course.").
33. James M. Swanson et al., Developmental Origins of Health & Disease: Environmental Exposures, 27 SEMINARS IN REPROD. MED. 391 (2009).
34. Matthew A. Maccani & Valerie S. Knopik, Cigarette Smoke Exposure-Associated Alterations to Non-Coding RNA, FRONTIERS GENETICS, Apr. 2012, at 1.
35. See generally Mariana Lagos-Quintana et al., Identification of Novel Genes Coding for Small Expressed RNAs, 294 SCIENCE 853 (2001).
36. As a general rule, perfect complementarity of a miRNA to its target mRNA sequence will result in the degradation of the mRNA transcript by a mechanism of Argonaute-catalyzed mRNA cleavage. See generally Gyorgy Hutvagner & Phillip D. Zamore, A microRNA in a Multiple-Turnover RNAi Enzyme Complex, 297 SCIENCE 2056 (2002);
37. Ji-Joon Song et al., Crystal Structure of Argonaute and Its Implications for RISC Slicer Activity, 305 Science 1434 (2004);
38. Soraya Yekta et al., MicroRNA-Directed Cleavage of HOXB8 mRNA, 304 SCIENCE 594 (2004).
39. Imperfect sequence complementarity between a miRNA and its target mRNA will result in the translational repression of the target mRNA by blocking or altering the function of translational machinery through mechanisms, including the inhibition of translation initiation and poly (A) shortening. See generally Witold Filipowicz et al., Mechanisms of Post-Transcriptional Regulation by microRNAs: Are the Answers in Sight?, 9 NATURE REVS. GENETICS 102 (2008);
40. Due to the fact that partial or imperfect complementarity of a miRNA to a target mRNA can lead to translational repression which can effectively silence a gene, a single miRNA has been observed and speculated to have the capability of regulating a large number of genes. See Tingting Du & Phillip D. Zamore, Beginning to Understand microRNA Function, 17 CELL RES. 661 (2007).
41. Some research has also pointed to the possibility that miRNA can utilize a combination of both translational repression and mRNA degradation as the mechanism for their posttranscriptional gene regulation, but more work is ongoing to more definitively characterize the mechanisms of miRNA-mediated regulation of gene expression. See generally Lee P. Lim et al., Microarray Analysis Shows That Some microRNAs Downregulate Large Numbers of Target mRNAs, 433 NATURE 769 (2005);
42. Matthew A. Maccani & Carmen J. Marsit, Exposure and Fetal Growth-Associated miRNA Alterations in the Human Placenta, 2 CLINICAL EPIGENETICS 401 (2011);
43. Genomic imprinting is the parent-of-origin, allele-specific expression of genes. Imprinted genes are theorized to be controlled by both non-coding RNAs and changes in DNA methylation at sites in differentially methylated regions ("DMRs"). During imprinting, DNA methylation functions to alter the binding of specific transcription factor or enhancer elements (or both) that control the allele specific expression of the region. See generally Miguel Constancia et al., Imprinting Mechanisms, 8 GENOME RES. 881 (1998);
44. Andrew J. Wood & Rebecca J. Oakey, Genomic Imprinting in Mammals: Emerging Themes and Established Theories, 2 PLoS GENETICS 1677 (2006). Imprinting has been hypothesized to be one of the mechanisms involved in the "parent conflict" theory. The "parent conflict theory" notes that paternally-expressed genes strongly promote the utilization of maternal resources to benefit offspring while maternally-expressed genes strongly promote the preservation of such maternal resources; thus, these parental influences are in direct conflict with one another. Using such logic, one might conclude that paternally-expressed (and maternally-imprinted) gene expression attempts to foster the growth of offspring while maternallyexpressed (and paternally-imprinted) gene expression tries to ensure that each offspring has approximately the same access to maternal resources as its siblings.
45. See generally C. Badcock & B. Crespi, Imbalanced Genomic Imprinting in Brain Development: An Evolutionary Basis for the Aetiology of Autism, 19 J. EVOLUTIONARY BIOLOGY 1007 (2006);
46. Shirley M. Tilghman, The Sins of the Fathers and Mothers: Genomic Imprinting in Mammalian Development, 96 CELL 185 (1999).
47. Genes regulated by imprinting are involved in a number of processes including embryonic and placental development and later-in-life functions such as behaviors and metabolism. Aberrant imprinting patterns have been described to lead to well-characterized syndromes (including Praeder-Willi and Angelman Syndromes), altered establishment of imprinted genes (particularly at chromosome 11p15), and Beckwith-Wiedemann Syndrome, which has also been linked to the use of assisted reproductive technologies. See generally Aimee S. Chang et al., Association Between Beckwith-Wiedemann Syndrome and Assisted Reproductive Technology: A Case Series of 19 Patients, 83 FERTILITY & STERILITY 349 (2005);
48. 19, 72 AM. J. HUM. GENETICS 156 (2003);
49. Anthony R. Isles & Anthony J. Holland, Imprinted Genes and Mother-Offspring Interactions, 81 EARLY HUM. DEV. 73 (2005);
50. E. R. Maher et al., Beckwith-Wiedemann Syndrome and Assisted Reproduction Technology (ART), 40 J. MED. GENETICS 62 (2003);
51. Benjamin Tycko & Ian M. Morison, Physiological Functions of Imprinted Genes, 192 J. CELL PHYSIOLOGY 245 (2002).
52. Histone modifications involve the acétylation, methylation, phosphorylation, and ubiquitination of histone proteins around which DNA is wrapped, leading to regulation of gene expression. See generally Atsushi P. Kimura et al., Epigenetic Modifications at the Human Growth Hormone Locus Predict Distinct Roles for Histone Acétylation and Methylation in Placental Gene Activation, 18 MOLECULAR ENDOCRINOLOGY 1018 (2004);
53. Bryan M. Turner, Cellular Memory and the Histone Code, 111 CELL 285 (2002).
54. Such modifications of the amino-terminal tails of core histones by acetylation, phosphorylation, and methylation can determine gene activity by altering the accessibility of DNA to factors which can lead to (or repress) gene expression. See Thomas Jenuwein & C. D. Allis, Translating the Histone Code, 293 SCIENCE 1074 (2001);
55. Brian D. Strahl & C. D. Allis, The Language of Covalent Histone Modifications, 403 NATURE 41 (2000);
56. Yi Zhang & Danny Reinberg, Transcription Regulation by Histone Methylation: Interplay Between Different Covalent Modifications of the Core Histone Tails, 15 GENES & DEV. 2343 (2001).
57. 3 Methyltransferase that Facilitates Transcription by Precluding Histone Tail Modifications Required for Heterochromatin Formation, 16 GENES & DEV. 479 (2002);
58. 0 Cells, 296 SCIENCE 1132 (2002);
59. 3 Methyltransferases, 406 NATURE 593 (2000);
60. 3, Lysine 9-Specific Methyltransferase that Contributes to HPI-Mediated Silencing of Euchromatic Genes by KRAB Zinc-Fmger Proteins, 16 GENES & DEV. 919 (2002);
61. 3-Lysine 4-Specific Methyltransferase, 8 MOLECULAR CELL 1027 (2001);
62. 3-Specific Methyltransferase that Interacts with ERG Transcription Factor, 21 ONCOGENE 148 (2002).
63. Researchers have also described a number of transcription co-activators that have characteristic histone acetyltransferase activity and histone deacetylases, which contribute to histone modification. See generally En Li, Chromatin Modification and Epigenetic Reprogramming in Mammalian Development, 3 NATURE REV. GENETICS 662 (2002). As a result, histone modifications can turn genes "on" or "off", depending on which modification has been made. Alterations to patterns of histone modification can have a number of consequences, such as developmental dysregulation and diseases. Research is continuing to explore how normal and altered histone modifications can control gene expression, as well as how such modifications might be involved in regulating additional epigenetic processes and disease states.
64. See generally Vincenzo Calvanese et al., Cancer Genes Hypermethylated in Human Embryonic Stem Cells, PLoS ONE, Sept. 2008, at 1.
65. Stella M. Reamon-Buettner et al., The Next Innovation Cycle in Toxicogenomics: Environmental Epigenetics, 659 MUTATION RES. 158, 159 (2008).
66. Matthew A. Maccani et al., Maternal Cigarette Smoking During Pregnancy Is Associated with Downregulation of miR-16, miR-21, and miR-i46a in the Placenta, 5 EPIGENETICS 583, 583 (2010).
67. Donna S. Lambers & Kenneth E. Clark, The Maternal and Fetal Physiologic Effects of Nicotine, 20 SEMINARS PERINATOLOGY 115, 119-21 (1996).
68. See generally John O. Beattie, Transplacental Alcohol Intoxication, 21 ALCOHOL & ALCOHOLISM 163 (1986).
69. See generally HJ. Guyda et al, Benio (a) pyrene Inhibits Epidermal Growth Factor Binding and Receptor Autophosphorylation in Human Placental Cell Cultures, 37 MOLECULAR PHARMACOLOGY 137, (1990).
70. Anne Castles et al., Effects of Smoking During Pregnancy: Five Meta-Analyses, 16 AM. J. PREVENTIVE MED. 208, 211 (1999).
71. Matthew A. Maccani et al., miR-16 and miR-21 Expression in the Placenta Is Associated with Fetal Growth, PLoS ONE, June 2011, at 1, 5.
72. Derek G. Cook & David P. Strachan, Summary of Effects of Parental Smoking on the Respiratory Health of Children and Implications for Research, 54 THORAX 357, 357 (1999).
73. See Susan L. Prescott & Vicki Clifton, Asthma and Pregnancy: Emerging Evidence of Epigenetic Interactions In Utero, 9 CURRENT OPINION IN ALLERGY & CLININCAL IMMUNOLOGY 417, 417 (2009).
74. S. P. Doherty et al., Early Life Insult From Cigarette Smoke May Be Predictive of Chronic Diseases Later in Life, 14 BIOMARKERS 97, 99-100 (2009).
75. Anja Thielen v et al., Tobacco Smoke: Unraveling a Controversial Subject, 60 EXPERIMENTAL & TOXICOLOGIC PATHOLOGY 141, 147 (2008).
76. See generally Niina Jaakkola et al., Smoking During Pregnancy in Finland: Determinants and Trends, 1987-1997, 91 AM. J. PUB. HEALTH 284 (2001);
77. U. S. DEP'T HEALTH & HUMAN SERVS., THE HEALTH CONSEQUENCES OF INVOLUNTARY EXPOSURE TO TOBACCO SMOKE: A REPORT OF THE SURGEON GENERAL (2006).
78. Sven Cnattingius, The Epidemiology of Smoking During Pregnancy: Smoking Prevalence, Maternal Characteristics, and Pregnancy Outcomes, 6 NICOTINE & TOBACCO RES. 125, 127 (2004).
79. See generally Renee D. Goodwin et al., Mental Disorders and Nicotine Dependence Among Pregnant Women in the United States, 109 OBSTETRICS & GYNECOLOGY 875 (2007).
80. See generally U. S. DEP'T HEALTH A HUMAN SERVS., supra note 77.
81. See generally Alison K. Shea & Meir Steiner, Cigarette Smoking During Pregnancy, 10 NICOTINE & TOBACCO RES. 267 (2008).
82. See generally Marie D. Cornelius & Nancy L. Day, Developmental Consequences of Prenatal Tobacco Exposure, 22 CURRENT OPINIONS IN NEUROLOGY 121 (2009).
83. See generally Melissa Suter et al., Maternal Tobacco Use Modestly Alters Correlated Epigenome-Wide Placental DNA Methylation and Gene Expression, 6 EPIGENETICS 1284 (2011).
84. See generally Melissa Suter et al. In Utero Tobacco Exposure Epigenetically Modifies Placental CYP1A1 Expression, 59 METABOLISM 1481 (2010).
85. See generally Charlotte S. Wilhelm-Benartzi et al., In Utero Exposures, Infant Growth, and DNA Methylation of Repetitive Elements and Developmentally Related Genes in Human Placenta, 120 ENVTL. HEALTH PERSP. 296 (2012).
86. See generally Y. Ba et al., Relationship of Folate, Vitamin B12 and Methylation of Insulin-Like Growth Factor-II in Maternal and Cord Blood, 65 EUR. J. CLINICAL NUTRITION 480 (2011).
87. See generally Mary Beth Terry et al, Genomic DNA Methylation Among Women in a Multiethnic New York City Birth Cohort, 17 CANCER EPIDEMIOLOGY, BIOMARKERS, & PREVENTION 2306 (2008).
88. Maria Toledo-Rodriguez et al., Maternal Smoking During Pregnancy Is Associated with Epigenetic Modifications of the Brain-Derived Neurotrophic Factor-6 Exon in Adolescent Offspring, 153 B AM. J. MED. GENETICS PT. B 1350, 1350-54 (2010).
89. See generally Eric J. Huang & Louis F. Reichardt, Neurotrophins: Roles in Neuronal Development and Function, 24 ANN. REV. NEUROSCIENCE 677 (2001).
90. See generally Manabu Fuchikami et al., DNA Methylation Profiles of the Brain-Derived Neurotrophic Factor (BDNF) Gene as a Potent Diagnostic Biomarker in Major Depression, PLoS ONE, Aug. 2011, at 1.
91. See generally Virender K. Rehan et al., Perinatal Nicotine Exposure Induces Asthma in Second Generation Offspring, 10 BMC MED. 129 (2012);
92. Grandma's Curse: Some of the Effects of Smoking May Be Passed From Grandmother to Grandchild, THE ECONOMIST, Nov. 3, 2012, at 82.
93. See generally Rodrigo Paz et al., Behavioral Teratogenicity Induced by Nonforced Maternal Nicotine Consumption, 32 NEUROPSYCHOPHARMACOLOGY 693 (2007).
94. See generally Barbara Maughan et al., Prenatal Smoking and Early Childhood Conduct Problems: Testing Genetic and Environmental Explanations of the Association, 61 ARCHTVES GEN. PSYCHIATRY 836 (2004).
95. See generally Jean Reith Schroedel et al., Women's Rights and Fetal Personhood in Criminal Law, 7 DUKE J. GENDER L. & POL'Y 89, 102 (2000).
96. Ada Calhoun, The Criminalization of Bad Mothers, N. Y. TIMES, Apr. 25, 2012, at MM30.
97. Cynthia Dailard & Elizabeth Nash, State Responses to Substance Abuse Among Pregnant Women, GUTTMACHER REP. PUB. POL'Y, Dec. 2000, at 1, 5.
98. See, e.g., Marilyn L. Poland et al., Punishing Pregnant Drug Users: Enhancing the Flight From Care, 31 DRUG & ALCOHOL DEPENDENCE 199, 202 (1993);
99. U. S. GEN. ACCOUNTING OFFICE, GAO/HRD-90-198, DRUG-EXPOSED INFANTS: A GENERATION AT RISK, at 9-10 (1990).
100. Whitner v. State, 492 S. E.2d 777, 778 (S. C. 1997).
101. Deborah Homstra, A Realistic Approach to Maternal-Fetal Conflict, 28 HASTINGS CTR. REP. 7, 10 (1998).
102. AM. SOC'Y ADDICTION MED., Public Policy Statement on Women, Alcohol and Other Drugs, and Pregnancy, 1 (July n, 2011), http://www.asam.org/docs/publicy- policy-statements/lwomenandpregnancy-7-11.pdf.
103. See generally Hermine H. Maes et al., A Twin Study of Genetic and Environmental Influences on Tobacco Initiation, Regular Tobacco Use and Nicotine Dependence, 34 PSYCHOL. MED. 1251 (2004).
104. Alison J. Wright et al., Is Attributing Smoking to Genetic Causes Associated with a Reduced Probability of Quit Attempt Success? A Cohort Study, 102 ADDICTION 1657, 1659 (2007).
105. Toby E. Jayaratne et al., The Perennial Debate: Nature, Nurture, or Choice? Black and White Americans' Explanations for Individual Differences, 13 REV. GEN. PSYCHOL. 24, 27 (2009).
106. Jo C. Phelan, Geneticization of Deviant Behavior and Consequences for Stigma: The Case of Mental Illness, 46 J. HEALTH & SOC. BEHAV. 307, 317 (2005).
107. Ilan Dar-Nimrod & Steven J. Heine, Genetic Essentialism: On the Deceptive Determinism of DNA, 137 PSYCHOL. BULL. 800, 802 (2011).
108. CTRS. FOR DISEASE CONTROL & PREVENTION, BEST PRACTICES FOR COMPREHENSIVE TOBACCO CONTROL PROGRAMS 7, 34 (2007).
109. Jennifer W. Kahende et al., A Review of Economic Evaluations of Tobacco Control Programs, 6 INT'L J. ENVTL. RES. & PUB. HEALTH 51, 54-63 (2009).
110. CTRS. FOR DISEASE CONTROL & PREVENTION, supra note 123, at 9.
111. Julia A. Dilley et al.. Program, Policy, and Price Interventions for Tobacco Control: Quantifying the Return on Investment of a State Tobacco Control Program, 102 AM. J. PUB. HEALTH 22, 24 (2012).
112. E. Kathleen Adams et al., Reducing Prenatal Smoking: The Role of State Policies, 43 AM. J. PREVENTIVE MED. 34, 39 (2012).
113. CTRS. FOR DISEASE CONTROL & PREVENTION, supra note 123, at 15. According to the CDC, best practices to reduce tobacco use were created from an "evidence-based analyses of scientific literature and outcomes of comprehensive state tobacco control programs and interventions."
114. CAMPAIGN FOR TOBACCO-FREE KIDS, BROKEN PROMISES TO OUR CHILDREN: THE 1998 STATE TOBACCO SETTLEMENT 14 YEARS LATER i (2012).
115. See, e.g., CAL. HEALTH & SAFETY CODE §§ 104555-58 (2000) (codifying California's adoption of the Master Settlement Agreement).
116. Sabrina Tavemise, States Cut Antismoking Outlays Despite Record Tobacco Revenue, N. Y. TIMES, Dec. 6, 2012, at A.19.
117. Adam J. Hoffer & Adam Pellillo, The Political Economy of Tobacco Control Spending, 19 APPLIED ECON. LETTERS 1793, 1795 (2012).
118. See generally CENTERS FOR DISEASE CONTROL & PREVENTION, supra note 123.
119. Jennifer Cantrell et al., Impact of Tobacco-Related Health Warning Labels Across Socioeconomic, Race and Ethnic Groups: Results from a Randomized Web-Based Experiment, PLoS ONE, Jan. 2013, at 1, 1;
120. Thomas N. Robinson & Joel D. Killen, Do Cigarette Warning Labels Reduce Smoking? Paradoxical Effects Among Adolescents, 151 ARCHIVES PEDIATRICS & ADOLESCENT MED. 267, 271-72 (1997).
121. David Hammond, Health Warning Messages on Tobacco Products: A Review, 20 TOBACCO CONTROL 327, 332 (2011);
122. David Hammond et al., Communicating Risk to Smokers: The Impact of Health Warnings on Cigarette Packages, 32 AM. J. PREVENTIVE MED. 1, 5-6 (2007).
123. Pub. L. No. 111-31, 123 Stat. 1776, 1777 (2009)
124. (codified as amended at 21 U. S. C. §§387-87u (2009)).
125. Cigarette Health Warnings, FOOD & DRUG ADMIN., http://www.fda.gov/ downloads/TobaccoProducts/Labeling/UCM259401.pdf (last visited July 30, 2013).
126. R. J. Reynolds Tobacco Co. v. FDA, 845 F. Supp. 2d 266, 277 (D. D. C. 2012).
127. R. J. Reynolds Tobacco Co. v. FDA, 696 F-3d 1205, 1222 (D. C. Cir. 2012).
128. See generally F. J. Chaloupka et al., Effectiveness of Tax and Price Policies in Tobacco Control, 20 TOBACCO CONTROL (2011).
129. See generally T. Coleman et al.. Pharmacological Interventions for Promoting Smoking Cessation During Pregnancy, 9 COCHRANE DATABASE SYSTEMATIC REVS. (2012).
130. Tim Stockwell et al., Does Minimum Pricing Reduce Alcohol Consumption? The Experience of a Canadian Province. 107 ADDICTION 912, 916 (2012).
131. See generally Jinhui Zhao et al., The Relationship Between Minimum Alcohol Prices, Outlet Densities and Alcohol Attributable Deaths in British Columbia, 2002-09, 108 ADDICTION 1059 (2013).
132. Leona Bull, et al., Social Attitudes Towards Smoking in Pregnancy in East Surrey: A Qualitative Study of Smokers, Former Smokers and Non-Smokers, 13 J. NEONATAL NURSING 100, 101 (2007).
133. See generally Joanne E. Callinan et al., Legislative Smoking Bans for Reducing Secondhand Smoke Exposure, Smoking Prevalence and Tobacco Consumption (Review), COCHRANE DATABASE SYSTEMATIC REVS. (2010).
134. Jerry M. Suis et al., Efficacy of Smoking-Cessation Interventions for Young Adults: A Meta-Analysis, 42 Am. J. PREVENTATIVE MED. 655, 660-61 (2012).
135. Lisa Sanderson Cox et al., Predictors of Early Versus Late Smoking Abstinence Within a 24-Month Disease Management Program, 13 NICOTINE & TOBACCO RES. 215, 218 (2011).
136. K. B. Filion et al., The Effect of Smoking Cessation Counselling in Pregnant Women: a Metaanalysis of Randomised Controlled Trials, 118 BJOG: INT'L J. OBSTETRICS & GYNAECOLOGY 1422, 1424 (2011).
137. See generally L. F. Stead & T. Lancaster, Combined Pharmacotherapy and Behavioural Interventions for Smoking Cessation, THE COCHRANE LIBR. (2012).
138. See generally Maria M. Morales-Suárez-Varela et al., Smoking Habits, Nicotine Use, and Congenital Malformations, 107 OBSTETRICS & GYNECOLOGY 51 (2006).
139. Valerie S. Knopik, Commentary: Smoking During Pregnancy-Genes and Environment Weigh In, 39 INT'L J. EPIDEMIOLOGY 1203, 1203-04 (2010).
140. Brian M. D'Onofrio et al., A Quasi-Experimental Study of Maternal Smoking During Pregnancy and Offspring Academic Achievement, 81 CHILD DEV. 80, 89 tbl.2 (2010).
141. Arpana Agrawal et al., Correlates of Cigarette Smoking During Pregnancy and its Genetic and Environmental Overlap with Nicotine Dependence, 10 NICOTINE & TOBACCO RES. 567, 573-76 (2008).
142. Valerie S. Knopik et al., Contributions of Parental Alcoholism, Prenatal Substance Exposure, and Genetic Transmission to Child ADHD Risk: A Female Twin Study, 35 PSYCHOL. MED. 625, 630 (2005).
143. Brian M. D'Onofrio et al., Familial Confounding of the Association Between Maternal Smoking During Pregnancy and Offspring Criminality: A Population-Based Study in Sweden, 67 ARCHIVES GEN. PSYCHIATRY 529, 532-33 (2010).
144. William D. Lopez et al., Abuse-Related Post-Traumatic Stress, Coping, and Tobacco Use in Pregnancy, 40 J. OBSTETRIC, GYNECOLOGIC & NEONATAL NURSING 422, 425 (2011).
145. See generally Kate E. Pickett et al., The Psychosocial Context of Pregnancy Smoking and Quitting in the Millennium Cohort Study, 63 J. EPIDEMIOLOGY & COMMUNITY HEALTH 474 (2009).
146. Peter Gluckman & Mark A. Hanson, Living with the Past: Evolution, Development, and Patterns of Disease, 305 SCIENCE 1733, 1733 (2004).
147. CTRS. FOR DISEASE CONTROL & PREVENTION, supra note 123, at 7, 34.