The DOI matches its Crossref record; 103 of the 103 references it cites were found in a registry or an index; 72 of the 131 sources its claims cite were checked for support.
Impact of Tobacco Smoke and Nicotine Exposure on Lung Development
Open accessAbstract
Review of tobacco smoke and nicotine effects on lung development.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
34 Supported · 34 No full text of the sources · 26 Partly supported · 15 Own interpretation · 6 No basis given · 5 Sources not found · 5 Not checked yet · 1 Supported so far · 1 Not supported · accuracy not yet measured
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Prenatal exposure of children to tobacco smoke remains high in the United States and worldwide, and caregiver questionnaires may underrepresent the actual number of children exposed to SHS. 6”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Tobacco Smoke Exposure in Children
What the sources say
- Partly supportedcites [6] Collaco, 2015, Hair nicotine levels in children with bronchopulmonary dysplasia, Pediatrics sourceExperimental — accuracy not yet measured
The Hair Nicotine Levels section reports that 21 of 93 children whose caregivers reported no household smoker had hair nicotine above the exposure cutoff, supporting the concern that questionnaires may miss exposed children. The study concerns young children with bronchopulmonary dysplasia; its Demographics section reports maternal smoking during pregnancy for three subjects, but it does not establish that prenatal tobacco-smoke exposure remains high in the United States or worldwide. (LLM, conf=0.90)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Tobacco smoke exposure can adversely affect lung development, cause small airway dysfunction and wheeze, and increase the frequency of upper and lower respiratory tract illnesses.[16][17][18]”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Abstract
What the sources say
- Could not verifycites [16] Suzuki, 2009, Association of environmental tobacco smoking exposure with an increased risk of hospital admissions for pneumonia in children under 5 years of age in Vietnam, Thorax sourceExperimental — accuracy not yet measured
The Significance of study section discusses smoke-related damage to respiratory defenses, and the Abstract discusses childhood respiratory illness, but neither addresses lung development. Searches for lung development and lung growth found no passage establishing that point in our copy. (LLM, conf=0.72)
- Not checked — no full text of the sourcecites [17] Kalliola, 2013, Maternal smoking affects lung function and airway inflammation in young children with multiple-trigger wheeze, J Allergy Clin Immunol source
- Supportedcites [18] Charoenca, 2013, Determining the burden of secondhand smoke exposure on the respiratory health of Thai children, Tob Induc Dis source
The Introduction states that secondhand smoke exposure impairs lung growth in children. That supports the attributed claim that tobacco smoke exposure can adversely affect lung development. (LLM, conf=0.91)
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Could not verify
Every source the paper cites for this claim was checked and supports it.
In the paper
“Prenatal exposure of children to tobacco smoke remains high in the United States and worldwide, and caregiver questionnaires may underrepresent the actual number of children exposed to SHS. 6”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Tobacco Smoke Exposure in Children
What the sources say
- Supportedcites [6] Collaco, 2015, Hair nicotine levels in children with bronchopulmonary dysplasia, Pediatrics source
In “Hair Nicotine Levels,” the paper reports that 21 of 93 children whose caregivers reported no household smoker had hair nicotine above the exposure cutoff. It concludes that clinic questionnaires may miss a substantial number of infants exposed to tobacco smoke. (LLM, conf=0.92)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“SHS exposure may also impair the effectiveness of corticosteroids used for the treatment of small airway disease.21”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Abstract
What the sources say
- Partly supportedcites [21] Cohen, 2010, In utero smoke exposure and impaired response to inhaled corticosteroids in children with asthma, J Allergy Clin Immunol sourceExperimental — accuracy not yet measured
The Results and Discussion report that children with asthma exposed to tobacco smoke in utero had a blunted response to inhaled budesonide. The claim extends that finding to SHS exposure generally and to treatment of small airway disease, neither of which the study establishes; current environmental tobacco smoke exposure was adjusted for, not identified as the exposure driving the result. Page numbers are unavailable in our copy. (LLM, conf=0.88)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In addition, adverse health effects caused by SHS may be augmented in children with a genetic susceptibility to asthma, and exposure to tobacco smoke during in utero life may cause epigenetic changes in fetal lung.22”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Abstract
What the sources say
- Partly supportedcites [22] Chhabra, 2014, Fetal lung and placental methylation is associated with in utero nicotine exposure, Epigenetics sourceExperimental — accuracy not yet measured
The Results and Discussion report an association between in utero nicotine exposure and altered DNA methylation in fetal lung, supporting the sentence’s epigenetic-change possibility. The paper does not establish that secondhand smoke has greater adverse effects in children genetically susceptible to asthma; its Introduction discusses prenatal smoke and asthma generally, while genotype appears in a reference title. (LLM, conf=0.86)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In addition, adverse health effects caused by SHS may be augmented in children with a genetic susceptibility to asthma, and exposure to tobacco smoke during in utero life may cause epigenetic changes in fetal lung.22”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Abstract
What the sources say
- Supportedcites [22] Chhabra, 2014, Fetal lung and placental methylation is associated with in utero nicotine exposure, Epigenetics source
The Abstract reports an association between in utero nicotine exposure, used as a likely surrogate for smoke exposure, and variable DNA methylation in fetal lung tissue. The Discussion describes methylation variation as a plausible result of smoke exposure, supporting the claim’s qualified “may cause” wording; the study does not establish causation. (LLM, conf=0.90)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“However, recently Chan and colleagues 19 found an association between childhood pneumonia and diminished adult lung function.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Abstract
What the sources say
- Supportedcites [19] Chan, 2015, Pneumonia in childhood and impaired lung function in adults: a longitudinal study, Pediatrics source
The Discussion reports that participants who had radiologically ascertained pneumonia before age 3 had lower FEV1:FVC ratios in their late 20s. The Conclusions likewise state that impaired airway function persisted into adult life. (LLM, conf=0.95)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The detrimental effects of childhood tobacco smoke exposure on respiratory health may be increased by other confounding factors, including psychosocial stress, lower socioeconomic status, underlying chronic lung disease, genetic polymorphisms, and exposure to environmental pollutants.20”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Abstract
What the sources say
- Partly supportedcites [20] Brehm, 2015, Stress and bronchodilator response in children with asthma, Am J Respir Crit Care Med sourceExperimental — accuracy not yet measured
The At a Glance Commentary and Abstract report that stress and an ADCYAP1R1 polymorphism are associated with reduced bronchodilator response in children with asthma. The Abstract says the analysis adjusted for environmental tobacco smoke; it does not show that stress or the polymorphism increases the respiratory harm from tobacco exposure. The cited passages also do not establish that lower socioeconomic status, chronic lung disease, or pollutants amplify that harm. Page numbers were not provided for these passages. (LLM, conf=0.83)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Tobacco smoke exposure can adversely affect lung development, cause small airway dysfunction and wheeze, and increase the frequency of upper and lower respiratory tract illnesses.[16][17][18]”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Abstract
What the sources say
- Partly supportedcites [16] Suzuki, 2009, Association of environmental tobacco smoking exposure with an increased risk of hospital admissions for pneumonia in children under 5 years of age in Vietnam, Thorax sourceExperimental — accuracy not yet measured
The Results report more pneumonia hospital admissions among children under 5 exposed to environmental tobacco smoke, supporting an association with a lower respiratory tract illness. The paper also discusses respiratory tract infections generally, but our copy does not establish an increased frequency of upper respiratory tract illnesses; its measured outcome was pneumonia admission. (LLM, conf=0.85)
- Not checked — no full text of the sourcecites [17] Kalliola, 2013, Maternal smoking affects lung function and airway inflammation in young children with multiple-trigger wheeze, J Allergy Clin Immunol source
- Partly supportedcites [18] Charoenca, 2013, Determining the burden of secondhand smoke exposure on the respiratory health of Thai children, Tob Induc Dis sourceExperimental — accuracy not yet measured
The Abstract Conclusions and Discussion link secondhand smoke exposure in Thai children to a greater risk of acute lower respiratory conditions. The paper does not establish an increase in upper respiratory illnesses or measure how frequently either type of illness occurs. (LLM, conf=0.88)
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In their study, exposure of nicotine caused downregulation of n-Myc expression and differentiation of nonhuman primate embryonic stem cells into fibroblasts, demonstrating that exposure to nicotine during embryogenesis can affect embryonic stem cell differentiation.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Normal Lung Development
What the sources say
- Partly supportedcites [29] Ben-Yehudah, 2013, Nicotine exposure during differentiation causes inhibition of N-myc expression, Respir Res sourceExperimental — accuracy not yet measured
The Results (Abstract; no page given) report that nonhuman primate embryonic stem cells differentiated into fibroblasts in the presence of nicotine, with reduced N-myc expression. But the Methods (In Vitro differentiation; no page given) describe a directed differentiation protocol used for both treated and untreated cells. The paper supports nicotine altering differentiation, not nicotine exposure causing the cells to differentiate into fibroblasts. (LLM, conf=0.90)
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
- It may state two separate claims as one. 20
- Probably not a substantial claim. 11
- The quote only partly states this claim. 1
At least one cited source doesn’t support this claim or points to a different paper, and none confirmed it — see the verdicts below.
In the paper
“Similarly, in a primate model, Wang and colleagues 66 demonstrated decreased Th1 cytokine production after in utero and postnatal smoke exposure, which correlated with decreased recruitment of Th1 immune cells to the lung parenchyma.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > SHS and Pulmonary Immune Responses
What the sources say
- Disputedcites [66] Wang, 2008, Effects of environmental tobacco smoke exposure on pulmonary immune response in infant monkeys, J Allergy Clin Immunol sourceExperimental — accuracy not yet measured
The paper reports reduced Th1-associated cytokine expression after perinatal smoke exposure. But the section ‘ETS effects on the recruitment of CXCR3-bearing immune cells in the lung’ reports fewer CXCR3-positive cells in the subepithelium, not the lung parenchyma; it says alveolar-tissue counts did not differ significantly among groups. (LLM, conf=0.88)
Checked by a reasoning model — may be wrong.
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Disputed
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Tobacco smoke exposure can adversely affect lung development, cause small airway dysfunction and wheeze, and increase the frequency of upper and lower respiratory tract illnesses.[16][17][18]”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Abstract
What the sources say
- Partly supportedcites [16] Suzuki, 2009, Association of environmental tobacco smoking exposure with an increased risk of hospital admissions for pneumonia in children under 5 years of age in Vietnam, Thorax sourceExperimental — accuracy not yet measured
The “Comparisons with other studies” section says environmental tobacco smoke exposure is related to wheeze in children. It does not address small-airway dysfunction or establish that exposure causes wheeze. Page numbers are unavailable in our copy. (LLM, conf=0.84)
- Not checked — no full text of the sourcecites [17] Kalliola, 2013, Maternal smoking affects lung function and airway inflammation in young children with multiple-trigger wheeze, J Allergy Clin Immunol source
- Partly supportedcites [18] Charoenca, 2013, Determining the burden of secondhand smoke exposure on the respiratory health of Thai children, Tob Induc Dis sourceExperimental — accuracy not yet measured
The Introduction (page unavailable) says secondhand smoke is a risk factor for asthma symptoms and impairs lung growth; the Discussion (page unavailable) links exposure in young Thai children to acute respiratory conditions, including bronchial asthma. The paper does not specifically report small-airway dysfunction or wheeze, so those outcomes are not fully supported by this source. (LLM, conf=0.79)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“A recent study of lung tissue from fetal and infant sudden death cases found a higher incidence of a7 nAChR immunostaining in lung associated with maternal smoking, and maternal smoking was linked to”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Normal Lung Development
What the sources say
- Supportedcites [41] Lavezzi, 2014, Possible role of the alpha7 nicotinic receptors in mediating nicotine's effect on developing lung - implications in unexplained human perinatal death, BMC Pulm Med source
The Results report a significant association between prenatal cigarette smoke exposure and lung hypoplasia, and identify hypoplasia of specific brainstem nuclei in the sudden-death cases, most of whose mothers smoked. The Conclusions describe an association among maternal smoking, lung hypoplasia, and developmental alterations of brainstem nuclei in these cases compared with controls. (LLM, conf=0.92)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Another study reported that Chinese school-aged children exposed to SHS had increased cough and reduced lung function compared with findings in unexposed children.52”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > SHS and Lung Function in Children
What the sources say
- Supportedcites [52] He, 2011, Environmental tobacco smoke exposure and Chinese schoolchildren's respiratory health: a prospective cohort study, Am J Prev Med source
The Results report more coughing at night among ETS-exposed children than unexposed children, and lower lung-function measures in certain exposed groups. The Abstract also concludes that ETS exposure was associated with impaired lung-function growth in Chinese school-aged children. The lung-function finding concerns specific airflow measures and exposure levels, rather than every measure in every exposed child. (LLM, conf=0.91)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Wongtrakool and colleagues 53 found an increase in a7 nAChRs and stimulated lung branching in nicotine-treated embryonic murine lung explants,”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > SHS and Lung Function in Children
What the sources say
- Partly supportedcites [53] Wongtrakool, 2007, Nicotine alters lung branching morphogenesis through the alpha7 nicotinic acetylcholine receptor, Am J Physiol Lung Cell Mol Physiol sourceExperimental — accuracy not yet measured
The Results report that nicotine stimulated branching in embryonic murine lung explants. They report higher α7 nAChR expression at certain developmental stages, but not an increase in receptor expression in the nicotine-treated explants; the Discussion attributes an increase following prenatal nicotine exposure to another study. (LLM, conf=0.88)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“suggesting that in utero nicotine exposure may lead to dysanaptic airway growth and reduced lung function in exposed offspring.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > SHS and Lung Function in Children
What the sources say
- Supportedcites [53] Wongtrakool, 2007, Nicotine alters lung branching morphogenesis through the alpha7 nicotinic acetylcholine receptor, Am J Physiol Lung Cell Mol Physiol source
The Abstract says nicotine-stimulated branching may contribute to dysanaptic lung growth and predispose the host to postnatal airway disease. The Discussion also links altered branching to decreased pulmonary function in offspring with prenatal nicotine exposure. The claim preserves the paper’s uncertainty with “may.” (LLM, conf=0.91)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Among the best understood and most consistently recovered changes in methylation patterns involves the AHRR gene, which encodes for the aryl hydrocarbon receptor repressor, a feedback inhibitor that has been suggested to attenuate effects of”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Epigenetic Effects of Tobacco Smoke Exposure
What the sources say
- Supportedcites [75] Monick, 2012, Coordinated changes in AHRR methylation in lymphoblasts and pulmonary macrophages from smokers, Am J Med Genet B Neuropsychiatr Genet source
The Discussion (page unavailable) describes AHRR as a feedback inhibitor of the aryl hydrocarbon receptor and says this modulation may moderate AHR’s role in oncogenesis and altered immune function. It also links the proposed feedback mechanism to smoking-induced AHR activity, supporting the claim’s hedged description of attenuation of smoke-related effects. (LLM, conf=0.85)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Cord blood studies have implicated smokinginduced methylation changes in multiple specific genes, including CYP1A1, GF1, FOXP3, and AHRR, [72][73][74] which play a role in detoxification and immune regulation and, therefore, may contribute to childhood lung disease.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Epigenetic Effects of Tobacco Smoke Exposure
What the sources say
- Partly supportedcites [72] Suter, 2010, In utero tobacco exposure epigenetically modifies placental CYP1A1 expression, Metabolism sourceExperimental — accuracy not yet measured
The Introduction (page not provided) reports smoking-associated hypomethylation of placental CYP1A1 and describes its role in processing tobacco-smoke compounds. The Discussion (page not provided) explicitly says the authors did not assay CYP1A1 or its promoter in fetal blood. This paper does not establish the other named genes’ roles in immune regulation or a contribution to childhood lung disease. (LLM, conf=0.90)
- Not checked — no full text of the sourcecites [73] 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 source
- Partly supportedcites [74] Joubert, 2012, 450K epigenome-wide scan identifies differential DNA methylation in newborns related to maternal smoking during pregnancy, Environ Health Perspect sourceExperimental — accuracy not yet measured
The Results and Discussion (pages unavailable in our copy) link maternal smoking to cord-blood methylation changes in CYP1A1, AHRR, and GFI1. The Discussion connects CYP1A1 and AHRR to detoxification, the AhR pathway to immune function, and GFI1 to development. It does not implicate FOXP3 or establish that these methylation changes contribute to childhood lung disease. (LLM, conf=0.87)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In animal models, exposure to in utero and early postnatal tobacco smoke has been associated with a Th1 and Th2 imbalance and an increased susceptibility to airway reactivity.31”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > SHS and Pulmonary Immune Responses
What the sources say
- Supportedcites [31] Singh, 2011, Prenatal secondhand cigarette smoke promotes Th2 polarization and impairs goblet cell differentiation and airway mucus formation, J Immunol source
The Introduction reports that prenatal plus early postnatal smoke exposure exacerbates allergic asthma in animal models, and identifies gestational exposure as the main driver of airway hyperreactivity and Th2 polarization. The Results sections also report increased airway hyperreactivity after prenatal exposure and suppression of the Th1-specific factor T-bet after prenatal or early postnatal exposure. The claim does not say that postnatal exposure alone increases airway reactivity. (LLM, conf=0.91)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Findings from animal models of prenatal and postnatal tobacco or nicotine exposure are relevant to human lung development and disease.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In animal models, exposure to in utero and early postnatal tobacco smoke has been associated with a Th1 and Th2 imbalance and increased susceptibility to lower respiratory tract infections.31”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > SHS and Pulmonary Immune Responses
What the sources say
- Supportedcites [31] Singh, 2011, Prenatal secondhand cigarette smoke promotes Th2 polarization and impairs goblet cell differentiation and airway mucus formation, J Immunol source
The Discussion (page unavailable) reports that prenatal smoke exposure promotes Th2 polarization and suppresses Th1 activation; it also reports Th1 suppression after early postnatal exposure. It says these changes may increase the risk of prolonged lung infections, while the Introduction reports exacerbated respiratory infections in mice exposed during early postnatal life. (LLM, conf=0.87)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Findings from animal models of prenatal and postnatal tobacco or nicotine exposure are relevant to human lung development and disease.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Wang and colleagues 66 examined the Th1 and Th2 pulmonary responses in lungs of infant monkeys exposed to in utero and early postnatal tobacco smoke”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > SHS and Pulmonary Immune Responses
What the sources say
- Supportedcites [66] Wang, 2008, Effects of environmental tobacco smoke exposure on pulmonary immune response in infant monkeys, J Allergy Clin Immunol source
The Abstract and Discussion report significantly reduced expression of IFN-g, its upstream regulators IL-12p70 and T-bet, and downstream IFN-g-inducible chemokines in infant monkeys exposed to tobacco smoke beginning in utero. The Animal treatment section confirms that exposure continued through early postnatal life. (LLM, conf=0.90)
plaindirect- Asserted: fails — The authors may not put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The authors may not put it forward as true. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. The quote only partly states this claim.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Recent animal studies in mice have shown an adverse effect of e-cigarette aerosols on postnatal lung development and the innate immune system.93,94”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Electronic Cigarettes and Lung Development
What the sources say
- Partly supportedcites [93] McGrath-Morrow, 2015, The effects of electronic cigarette emissions on systemic cotinine levels, weight and postnatal lung growth in neonatal mice, PLoS One sourceExperimental — accuracy not yet measured
The Discussion (page unavailable) reports modestly impaired postnatal alveolar growth in neonatal mice exposed to nicotine-containing e-cigarette emissions. The paper does not report an adverse effect on the innate immune system; its immunohistochemistry measured Ki67 as a marker of cell proliferation, not immune function. (LLM, conf=0.90)
- Partly supportedcites [94] Sussan, 2015, Exposure to electronic cigarettes impairs pulmonary anti-bacterial and anti-viral defenses in a mouse model, PLoS One sourceExperimental — accuracy not yet measured
The Results section on pulmonary anti-bacterial defenses reports impaired bacterial phagocytosis by alveolar macrophages after e-cigarette exposure, supporting an adverse effect on innate immune defenses. The Methods (Animals; no page available) identify the mice as 8 weeks old, and the paper does not report an effect on postnatal lung development. (LLM, conf=0.90)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In a well-established animal model of in utero nicotine exposure, Rehan and colleagues 81 demonstrated increased airway resistance and contractility proteins in rats that were one generation (F2) removed from in utero nicotine exposure, which was supported by tissuespecific epigenetic differences.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Epigenetic Effects of Tobacco Smoke Exposure
What the sources say
- Supportedcites [81] Rehan, 2012, Perinatal nicotine exposure induces asthma in second generation offspring, BMC Med source
The Results report increased airway resistance in F2 rats despite no nicotine exposure during the F1 pregnancy, and increased contractile-protein levels in F2 lung tissue. The Results also describe distinct nicotine-associated DNA methylation and histone-acetylation changes in lung, testes, and ovaries, supporting the reference to tissue-specific epigenetic differences. Page numbers were not supplied in our copy. (LLM, conf=0.91)
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Findings from animal models of prenatal and postnatal tobacco or nicotine exposure are relevant to human lung development and disease.
- Supported
In the paper
“In the United States, an estimated 400,000 newborns are exposed every year to tobacco smoke during pregnancy, with 10.7% of pregnant mothers smoking during the last 3 months of pregnancy.23”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Tobacco Smoke Exposure in Children
What the sources say
- Not matchedcites [23] Tong, 2013, Trends in smoking before, during, and after pregnancy–Pregnancy Risk Assessment Monitoring System, United States, 40 sites, 2000-2010, MMWR Surveill Summ
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
In the paper
“Analysis from the Pregnancy Risk Assessment Monitoring System for 2001 and 2002 revealed that maternal smoking was associated with a longer length of stay in the neonatal intensive care unit, with an estimated smoking-attributable cost of $122 million annually in the United States.26”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Tobacco Smoke Exposure in Children
What the sources say
- Not checked — no full text of the sourcecites [26] Adams, 2011, Infant delivery costs related to maternal smoking: an update, Nicotine Tob Res source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“In the United States, an estimated 400,000 newborns are exposed every year to tobacco smoke during pregnancy, with 10.7% of pregnant mothers smoking during the last 3 months of pregnancy.23”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Tobacco Smoke Exposure in Children
What the sources say
- Not matchedcites [23] Tong, 2013, Trends in smoking before, during, and after pregnancy–Pregnancy Risk Assessment Monitoring System, United States, 40 sites, 2000-2010, MMWR Surveill Summ
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
In the paper
“The highest prevalence of smoking has been reported in women between 20 and 24 years of age (17.6%).23”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Tobacco Smoke Exposure in Children
What the sources say
- Not matchedcites [23] Tong, 2013, Trends in smoking before, during, and after pregnancy–Pregnancy Risk Assessment Monitoring System, United States, 40 sites, 2000-2010, MMWR Surveill Summ
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
In the paper
“Oberg and colleagues, 27 using data from 192 countries in 2004 reported that 40% of children worldwide were exposed to SHS.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Tobacco Smoke Exposure in Children
What the sources say
- Not checked — no full text of the sourcecites [27] Oberg, 2011, Worldwide burden of disease from exposure to second-hand smoke: a retrospective analysis of data from 192 countries, Lancet source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“They also estimated that 5,939,000 lower respiratory tract infections in children younger than 5 years were because of SHS exposure and that 28% of the approximately 379,000 deaths annually”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Tobacco Smoke Exposure in Children
What the sources say
- Not checked — no full text of the sourcecites [27] Oberg, 2011, Worldwide burden of disease from exposure to second-hand smoke: a retrospective analysis of data from 192 countries, Lancet source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“In utero tobacco and nicotine exposure remains common, occurring in approximately 10% of pregnancies within the United States.”
- Also stated in: § Tobacco Smoke Exposure in Children · hedged
“In the United States, an estimated 400,000 newborns are exposed every year to tobacco smoke during pregnancy, with 10.7% of pregnant mothers smoking during the last 3 months of pregnancy.23”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Abstract
What the sources say
- Not matchedcites [23] Tong, 2013, Trends in smoking before, during, and after pregnancy–Pregnancy Risk Assessment Monitoring System, United States, 40 sites, 2000-2010, MMWR Surveill Summ
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Also stated in: § Tobacco Smoke Exposure in Children · hedged
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“In utero nicotine exposure has been reported to disrupt normal developmental processes in the brain and lungs.36,37”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Normal Lung Development
What the sources say
- Not checked — no full text of the sourcecites [36] Smith, 2010, Early exposure to nicotine during critical periods of brain development: mechanisms and consequences, J Pediatr Biochem source
- Not checked — no full text of the sourcecites [37] Maritz, 2013, Perinatal exposure to nicotine and implications for subsequent obstructive lung disease, Paediatr Respir Rev source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Both in utero and postnatal SHS exposure have been associated with increased respiratory symptoms or reduced lung function in exposed children.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > SHS and Lung Function in Children
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Observed associations between tobacco smoke exposure and childhood respiratory outcomes reflect causal effects of tobacco smoke or nicotine.
In the paper
“They also estimated that 5,939,000 lower respiratory tract infections in children younger than 5 years were because of SHS exposure and that 28% of the approximately 379,000 deaths annually”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Tobacco Smoke Exposure in Children
What the sources say
- Not checked — no full text of the sourcecites [27] Oberg, 2011, Worldwide burden of disease from exposure to second-hand smoke: a retrospective analysis of data from 192 countries, Lancet source
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Along with modifying infection risk, the SHS-skewed immune response toward a Th2 bias may result in an allergic phenotype, small airway inflammation, and asthmalike symptoms.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > SHS and Pulmonary Immune Responses
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Epigenetic modification of gene expression and phenotype plays an important role in fetal development; furthermore, the epigenome that develops in utero and in early life persists throughout life and is heritable.67”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Epigenetic Effects of Tobacco Smoke Exposure
What the sources say
- Not checked — no full text of the sourcecites [67] Reik, 2007, Stability and flexibility of epigenetic gene regulation in mammalian development, Nature source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, smoke exposure may render neonates vulnerable to infection and promote development of allergic disease by changing the activation profile of immune cells.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Th2 Th1
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Tobacco-related epigenetic changes, particularly DNA methylation, were first noted in the context of cancer development and progression.68,69”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Epigenetic Effects of Tobacco Smoke Exposure
What the sources say
- Not checked — no full text of the sourcecites [68] Belinsky, 2002, Aberrant promoter methylation in bronchial epithelium and sputum from current and former smokers, Cancer Res
- Not checked — no full text of the sourcecites [69] Russo, 2005, Differential DNA hypermethylation of critical genes mediates the stage-specific tobacco smoke-induced neoplastic progression of lung cancer, Clin Cancer Res source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“The first study to associate in utero smoke and GST enzymes found that GSTM1 null children had increased risk of both diagnosed asthma and wheezing after in utero smoke exposure compared with findings in individuals with functional copies.87”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Gene-Environment Interactions and Tobacco Smoke Exposure
What the sources say
- Not checked — no full text of the sourcecites [87] Gilliland, 2002, Effects of glutathione S-transferase M1, maternal smoking during pregnancy, and environmental tobacco smoke on asthma and wheezing in children, Am J Respir Crit Care Med source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Glutathione S-transferase enzymes play a role in metabolizing tobacco products and reactive oxygen species.
In the paper
“A recent study from the United Kingdom reported that offspring of mothers given nicotine replacement therapy during their first trimester or a month prior to conception had a significant increase in respiratory anomalies but not in any other organ-specific system.96”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Electronic Cigarettes and Lung Development
What the sources say
- Not checked — no full text of the sourcecites [96] Dhalwani, 2015, Nicotine replacement therapy in pregnancy and major congenital anomalies in offspring, Pediatrics source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Ultimately, tobacco smoke-related modification of the epigenome appears to have longitudinal effects on DNA methylation patterns and may even alter transgenerational risk for the development of lung disease.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Epigenetic Effects of Tobacco Smoke Exposure
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper relies on this without support.
Findings from animal models of prenatal and postnatal tobacco or nicotine exposure are relevant to human lung development and disease.
“Animal models, however, support immune cell phenotypic changes after in utero smoke and nicotine exposure (Fig 1).”
The paper relies on this without support.
Observed associations between tobacco smoke exposure and childhood respiratory outcomes reflect causal effects of tobacco smoke or nicotine.
“Tobacco smoke exposure during prenatal and postnatal lung development is associated with an increase in respiratory morbidities during childhood.”
“Tobacco smoke and nicotine exposure during prenatal and postnatal life can impair lung development, alter the immune response to viral infections, and increase the prevalence of wheezing during childhood.”
The paper relies on this without support.
Nicotine is a key mediator of the adverse effects of tobacco smoke on lung development.
“Although multiple tobacco toxins likely affect the fetus, nicotine is the best studied component of tobacco smoke.”
“This review examines the impact of prenatal tobacco and nicotine exposure on lung development with a particular focus on nicotinic acetylcholine receptors.”
The paper relies on this without support.
DNA methylation changes measured in cord blood or placenta reflect functionally relevant changes in lung tissue.
“Because of difficulties in sampling, the majority of epigenetic studies of fetal methylation patterns in humans have been performed in cord blood and placenta.”
“Significant variability in methylation patterns between cord blood and placental and saliva samples suggests tissue-specific epigenetic patterns, 79 which may lead to differing functional consequences.80”
The paper relies on this without support.
Electronic nicotine delivery systems have the capacity to deliver a high level burst of nicotine.
“However, electronic nicotine delivery systems have the capacity to deliver a high level burst of nicotine.”
The paper relies on this without support.
Glutathione S-transferase enzymes play a role in metabolizing tobacco products and reactive oxygen species.
“Encoding for the glutathione S-transferase enzymes, GSTs play a role in metabolizing tobacco products and reactive oxygen species.”
The paper relies on this without support.
Electronic nicotine delivery systems have increased in popularity among people of childbearing age.
“With the increased popularity of electronic nicotine delivery systems among people of childbearing age, it is unknown what effect nicotine-containing e-cigarette aerosols will have on the lung function and respiratory health of children exposed during in utero and early postnatal life.”
Citations
Cites
Stability and flexibility of epigenetic gene regulation in mammalian development
Reik, W. (2007) · Nature · doi:10.1038/nature05918 · Cited by 1,963 · cited 1×
“Epigenetic modification of gene expression and phenotype plays an important role in fetal development; furthermore, the epigenome that develops in utero and in early life persists throughout life and is heritable.(67)”
BackgroundÖberg, M., Jaakkola, M. S., Woodward, A., Peruga, A., & Prüss-Ustün, A. (2011) · The Lancet · doi:10.1016/s0140-6736(10)61388-8 · Cited by 1,939
Tobacco smoking leads to extensive genome-wide changes in DNA methylation
Zeilinger, S., Kühnel, B., Klopp, N., Baurecht, H., Kleinschmidt, A., Gieger, C., Weidinger, S., Lattka, E., Adamski, J., Peters, A., et al. (2013) · PLoS ONE · doi:10.1371/journal.pone.0063812 · Cited by 824
Joubert, B. R., Håberg, S. E., Nilsen, R. M., Wang, X., Vollset, S. E., Murphy, S. K., Huang, Z., Hoyo, C., Midttun, Ø., Cupul-Uicab, L. A., et al. (2012) · Environmental Health Perspectives · doi:10.1289/ehp.1205412 · Cited by 716
Lerner, C. A., Sundar, I. K., Yao, H., Gerloff, J., Ossip, D. J., McIntosh, S., Robinson, R., & Rahman, I. (2015) · PLOS ONE · doi:10.1371/journal.pone.0116732 · Cited by 666
Tobacco-smoking-related differential DNA methylation: 27K discovery and replication
Breitling, L. P., Yang, R., Korn, B., Burwinkel, B., & Brenner, H. (2011) · The American Journal of Human Genetics · doi:10.1016/j.ajhg.2011.03.003 · Cited by 640
Tong, V. T., Dietz, P. M., Morrow, B., D’Angelo, D. V., Farr, S. L., Rockhill, K. M., & England, L. J. (2009) · PubMed · Cited by 617
Thurlbeck, W. M. (1982) · Thorax · doi:10.1136/thx.37.8.564 · Cited by 610
Gilliland, F. D., Li, Y., & Peters, J. M. (2001) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/ajrccm.163.2.2006009 · Cited by 569
Fetal and Postnatal Development of the Lung
Burri, P. H. (1984) · Annual Review of Physiology · doi:10.1146/annurev.ph.46.030184.003153 · Cited by 495
Cited by
Sorted by citations
Strzelak, A., Ratajczak, A., Adamiec, A., & Feleszko, W. (2018) · International Journal of Environmental Research and Public Health · doi:10.3390/ijerph15051033 · Cited by 557
“However, prenatal nicotine exposure was reported to alter normal lung development through upregulation of nicotinic acetylcholine receptors (nAChRs) expressed in the lung and brain during early fetal life [42].”
BackgroundAsthma epidemiology and risk factors
Stern, J. L., Pier, J., & Litonjua, A. A. (2020) · Seminars in Immunopathology · doi:10.1007/s00281-020-00785-1 · Cited by 612
Vanker, A., Gie, R. P., & Zar, H. J. (2017) · Expert Review of Respiratory Medicine · doi:10.1080/17476348.2017.1338949 · Cited by 183
“[14] Animal models suggest that 62 nicotine is the component that has significant detrimental effects on lung growth 63 and collagen deposition.”
BackgroundChen, H., Li, G. E., Chan, Y., Chapman, D. G., Sukjamnong, S., Nguyen, T., Annissa, T. F., McGrath, K., Sharma, P., & Oliver, B. (2017) · American Journal of Respiratory Cell and Molecular Biology · doi:10.1165/rcmb.2017-0206rc · Cited by 135
“It has been well accepted that tobacco smoke and nicotine exposure during prenatal and postnatal life can impair lung development (21).”
Solaligue, D. E. S., Rodríguez‐Castillo, J. A., Ahlbrecht, K., & Morty, R. E. (2017) · American Journal of Physiology-Lung Cellular and Molecular Physiology · doi:10.1152/ajplung.00343.2017 · Cited by 149
Metadata
- Authors
- Gibbs, K., Collaco, J. M., & McGrath-Morrow, S. A.
- Affiliations
- Johns Hopkins University (US)
- Venue
- Chest
- Publisher
- Elsevier BV
- Published
- 2016-02
- Volume
- 149
- Issue
- 2
- Pages
- 552-561
- ISSN
- 0012-3692 (ISSN-L)
- PMC
- PMC4944770
- OpenAlex
- W1924005154
- Cited by
- 201
- References
- 102
- Citations by year
- 2026: 11 · 2025: 14 · 2024: 13 · 2023: 21 · 2022: 26 · 2021: 17 · 2020: 35 · 2019: 18 · 2018: 19 · 2017: 18 · 2016: 9
- FWCI
- 1.88
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- CHEST Journal (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Flight Attendant Medical Research Institute
- National Institutes of Health
- National Heart, Lung, and Blood Institute (R01HL114800)
- Topics
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Smoking Behavior and Cessation
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Asthma and respiratory diseases
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Prenatal Substance Exposure Effects
- Keywords
- tobacco smoke exposure, nicotine exposure, lung development, prenatal tobacco exposure, passive smoking, wheezing, asthma, respiratory infection susceptibility, Th2 immune response, allergic phenotype, nicotinic acetylcholine receptors, DNA methylation, epigenetics, lung function, genetic risk factors
- MeSH terms
- Female, Humans, Infant, Newborn, Lung, Nicotine, Pregnancy, Prenatal Exposure Delayed Effects, Tobacco Smoke Pollution
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.
A language model drew the claims from the paper on 2026-10-11, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-11 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
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 ›
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