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
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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
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“A recent randomized placebo-controlled study found that the offspring of smoking mothers who received vitamin C during in utero life had better airflow and less wheezing through the first year of life compared with those of untreated mothers who smoked during pregnancy.43”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Normal Lung Development
What the sources say
- Partly supportedcites [43] McEvoy, 2014, Vitamin C supplementation for pregnant smoking women and pulmonary function in their newborn infants: a randomized clinical trial, JAMA sourceExperimental — accuracy not yet measured
The Results report improved pulmonary function in newborns of smokers randomized to vitamin C and less wheezing through the first year compared with the placebo group. But the Secondary Outcomes section reports no significant difference in pulmonary function at one year, so the source does not establish better airflow throughout that year. (LLM, conf=0.86)
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.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Prenatal nicotine exposure in mice has been shown to lead to diminished forced expiratory flows in adulthood, but interestingly not in a7 nAChR knockout mice.38”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Normal Lung Development
What the sources say
- Supportedcites [38] Wongtrakool, 2012, Prenatal nicotine exposure alters lung function and airway geometry through alpha7 nicotinic receptors, Am J Respir Cell Mol Biol source
The Results report decreased forced expiratory flows in nicotine-exposed mice and no such decrease in α7 nAChR knockout mice. The Materials and Methods describe pulmonary-function testing in 8-week-old mice, supporting the adulthood qualifier. The exposure model included gestation and early postnatal life, rather than gestation alone. (LLM, conf=0.91)
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.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Prenatal nicotine exposure in mice has been shown to lead to diminished forced expiratory flows in adulthood, but interestingly not in a7 nAChR knockout mice.38”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Normal Lung Development
What the sources say
- Supportedcites [38] Wongtrakool, 2012, Prenatal nicotine exposure alters lung function and airway geometry through alpha7 nicotinic receptors, Am J Respir Cell Mol Biol source
The Results (page unavailable) report decreased forced expiratory flows in nicotine-exposed mice but no such decrease in mice lacking α7 nAChR. The study’s exposure model included gestation and early postnatal life, a qualification to the citing sentence’s shorthand description as prenatal exposure. (LLM, conf=0.92)
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.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Rodent studies have indicated that nicotine exposure during prenatal life may alter central and peripheral respiratory chemoreception.46,47”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Maternal Smoking and Sudden Infant Death Syndrome
What the sources say
- Partly supportedcites [46] Cerpa, 2015, The alteration of neonatal raphe neurons by prenatal-perinatal nicotine. Meaning for sudden infant death syndrome, Am J Respir Cell Mol Biol sourceExperimental — accuracy not yet measured
The Abstract reports that prenatal–perinatal nicotine exposure reduces central respiratory chemoreception in neonatal mice, and the study found a diminished ventilatory response to hypercapnia. Our copy does not establish an effect on peripheral respiratory chemoreception; its mention of reduced responses to hypoxia does not identify a peripheral mechanism. (LLM, conf=0.86)
- Not checked — no full text of the sourcecites [47] Mahliere, 2008, Prenatal nicotine alters maturation of breathing and neural circuits regulating respiratory control, Respir Physiol Neurobiol source
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.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Hayatbakhsh and colleagues 51 also found that men with prior in utero smoke exposure had significant reductions in FEV 1 and midexpiratory flow.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > SHS and Lung Function in Children
What the sources say
- Supportedcites [51] Hayatbakhsh, 2009, Maternal smoking during and after pregnancy and lung function in early adulthood: a prospective study, Thorax source
The ‘Maternal smoking and young adult lung function’ results report statistically significant reductions in both FEV1 and FEF25–75 among male participants exposed to maternal smoking during pregnancy. FEF25–75 is the midexpiratory-flow measure in the claim. (LLM, conf=0.94)
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.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Another study reported that neonatal mice exposed to nicotine in utero had decreased ventilation and a reduced response to hypercarbia when exposed to 100% nitrogen for 20 seconds and 10% CO 2 for 20 minutes.49”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Maternal Smoking and Sudden Infant Death Syndrome
What the sources say
- Supportedcites [49] Eugenin, 2008, Prenatal to early postnatal nicotine exposure impairs central chemoreception and modifies breathing pattern in mouse neonates: a probable link to sudden infant death syndrome, J Neurosci source
The Materials and Methods describe nicotine delivery beginning during gestation. The breathing-pattern results report lower basal minute ventilation in P0–P1 exposed pups, while the hypoxia and hypercarbia results report reduced responses in P0–P3 pups under the stated 100% N₂ and 10% CO₂ protocols. The exposure continued into early postnatal life, which the citing sentence does not mention. (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.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“They also found that nicotine increased expression of a7 receptors in airway cartilage and vessels of fetal lung and that other nicotinic receptor subtypes, although expressed in fetal lung, were not upregulated by nicotine.30”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Normal Lung Development
What the sources say
- Supportedcites [30] Sekhon, 1999, Prenatal nicotine increases pulmonary alpha7 nicotinic receptor expression and alters fetal lung development in monkeys, J Clin Invest source
The Nicotinic receptor immunohistochemistry section reports that antibodies recognizing non-α7 subunits stained cells in the developing fetal lung, with no major difference in staining intensity after nicotine treatment (Fig. 4). This supports the claim for the other receptor subtypes examined; it does not establish a result for every possible subtype. (LLM, conf=0.88)
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.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“They also found that nicotine increased expression of a7 receptors in airway cartilage and vessels of fetal lung and that other nicotinic receptor subtypes, although expressed in fetal lung, were not upregulated by nicotine.30”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Normal Lung Development
What the sources say
- Supportedcites [30] Sekhon, 1999, Prenatal nicotine increases pulmonary alpha7 nicotinic receptor expression and alters fetal lung development in monkeys, J Clin Invest source
The Nicotinic receptor immunohistochemistry section reports markedly increased α7 staining in cartilaginous airway walls and blood vessel walls of nicotine-exposed fetal monkeys. It also reports expression of other nicotinic receptor subunits in developing lung, with no major difference in their staining intensity after nicotine treatment. (LLM, conf=0.91)
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.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Sekhon and colleagues 30 implanted nicotine pumps in pregnant rhesus monkeys and found reduced total body weight and alveolar hypoplasia in the offspring.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Normal Lung Development
What the sources say
- Supportedcites [30] Sekhon, 1999, Prenatal nicotine increases pulmonary alpha7 nicotinic receptor expression and alters fetal lung development in monkeys, J Clin Invest source
The Introduction reports that prenatal nicotine caused lung hypoplasia and reduced the surface complexity of developing alveoli. The Results state that pregnant rhesus monkeys received nicotine through implanted pumps and that fetal body weight was 8% lower than in controls, although the reduction was not statistically significant. The Discussion describes larger primitive alveoli, reduced surface area, and potentially fewer airspaces. (LLM, conf=0.91)
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.
- 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 Abstract Results report significantly more strong α7 nAChR immunostaining in lung cells and vessel walls of sudden fetal and infant death cases with smoker mothers. The Results section also reports a significant association between strong α7 expression and prenatal cigarette-smoke exposure. (LLM, conf=0.94)
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.
- Supported
Every source the paper cites for this claim was checked and supports it.
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
- Supportedcites [29] Ben-Yehudah, 2013, Nicotine exposure during differentiation causes inhibition of N-myc expression, Respir Res source
The Abstract Results report that nonhuman primate embryonic stem cells differentiated in the presence of nicotine had decreased N-myc mRNA and protein expression. The Discussion likewise states that N-myc expression was decreased in the nicotine-exposed group. (LLM, conf=0.94)
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.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Sekhon and colleagues 30 implanted nicotine pumps in pregnant rhesus monkeys and found reduced total body weight and alveolar hypoplasia in the offspring.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Normal Lung Development
What the sources say
- Supportedcites [30] Sekhon, 1999, Prenatal nicotine increases pulmonary alpha7 nicotinic receptor expression and alters fetal lung development in monkeys, J Clin Invest source
The Results report that nicotine administration reduced fetal body weight by 8% compared with controls, although the small sample precluded statistical significance. The Experimental design describes nicotine pumps implanted in pregnant rhesus monkeys, and the Discussion reports lung hypoplasia with reduced complexity of the gas-exchange surface. (LLM, conf=0.92)
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.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Since the 1980s, studies have demonstrated increased risk for lower respiratory tract infections in infants exposed to maternal smoke.56,57”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > SHS Exposure and Childhood Respiratory Infections
What the sources say
- Supportedcites [56] Fergusson, 1980, Parental smoking and respiratory illness in infancy, Arch Dis Child source
The Abstract and Discussion report that infants of mothers who smoked had an increased risk of lower respiratory illness, including illness affecting the lower respiratory tract. The paper distinguishes this from their overall risk of respiratory infection, which was similar to that of infants of nonsmoking mothers. (LLM, conf=0.91)
- Supportedcites [57] Taylor, 1987, Maternal smoking during pregnancy and lower respiratory tract illness in early life, Arch Dis Child source
The Results report that maternal smoking during pregnancy was associated with increased lower respiratory tract illness, including bronchitis and hospital admissions. The paper also reports that the effect was evident in the first year of life, supporting the claim about infants. (LLM, conf=0.87)
boostedcorrelational- 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
“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
- Supportedcites [29] Ben-Yehudah, 2013, Nicotine exposure during differentiation causes inhibition of N-myc expression, Respir Res source
The Methods (no page given) describe treating nonhuman primate embryonic stem cells with nicotine during differentiation. The Discussion (no page given) says these cells model development and that nicotine exposure could affect early embryonic differentiation. The evidence comes from an in vitro model, not direct exposure of embryos. (LLM, conf=0.91)
boostedconditional- 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
“A 2012 study found that maternal smoking was reported in 38.6% of infants dying of SIDS.44”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Maternal Smoking and Sudden Infant Death Syndrome
What the sources say
- Partly supportedcites [44] Trachtenberg, 2012, Risk factor changes for sudden infant death syndrome after initiation of Back-to-Sleep campaign, Pediatrics sourceExperimental — accuracy not yet measured
The Results table reports maternal smoking in 78 SIDS cases (38.6%) during the 1996–2008 Back-to-Sleep era. The claim omits that this percentage applies to that period, rather than to all SIDS cases in the study. (LLM, conf=0.88)
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.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“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”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Epigenetic Effects of Tobacco Smoke Exposure
What the sources say
- Supportedcites [80] Lokk, 2014, DNA methylome profiling of human tissues identifies global and tissue-specific methylation patterns, Genome Biol source
The Conclusions state that distinctive tissue methylation patterns reflect tissue-specific functions and that tissue-specific differentially methylated regions are enriched for genes related to those functions. This supports the hedged claim that tissue-specific epigenetic patterns may have differing functional consequences. (LLM, conf=0.90)
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.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Subsequently, epigenetic differences in global DNA methylation have been found between smokers and nonsmokers.70,71”
§ 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 [70] Breitling, 2011, Tobacco-smoking-related differential DNA methylation: 27K discovery and replication, Am J Hum Genet source
- Partly supportedcites [71] Zeilinger, 2013, Tobacco smoking leads to extensive genome-wide changes in DNA methylation, PLoS One sourceExperimental — accuracy not yet measured
The Results and Discussion section reports 972 differentially methylated CpG sites across the genome, including 187 replicated sites, when comparing current with never smokers. That supports widespread site-specific differences, but the paper does not report a difference in global DNA methylation as an overall measure. (LLM, conf=0.84)
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.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Sumino and colleagues 62 correlated decreased monocyte interferon production at birth with increased risk of early life infection.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > SHS and Pulmonary Immune Responses
What the sources say
- Partly supportedcites [62] Sumino, 2012, Antiviral IFN-gamma responses of monocytes at birth predict respiratory tract illness in the first year of life, J Allergy Clin Immunol sourceExperimental — accuracy not yet measured
The Discussion reports that lower RSV-induced IFNG mRNA in cord-blood monocytes at birth was associated with more respiratory tract illness during the first year of life in infants at high risk for asthma and allergic disease. The claim broadens this to early-life infection generally; the Discussion says the response was not linked to some other types of infection. The measured response was IFNG mRNA, rather than interferon protein production. (LLM, conf=0.88)
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Placental studies also have demonstrated changes in global and gene-specific methylation.78”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Epigenetic Effects of Tobacco Smoke Exposure
What the sources say
- Partly supportedcites [78] Maccani, 2015, Altered placental DNA methylation patterns associated with maternal smoking: current perspectives, Adv Genomics Genet sourceExperimental — accuracy not yet measured
The Conclusion and future directions reports gene-specific placental methylation changes associated with maternal smoking, but says epigenome-wide changes may occur only “perhaps, to a lesser degree.” Genetic pathways associated with MCSDP reports changes in repetitive-element methylation associated with epigenome-wide patterns. These passages support gene-specific changes but are more cautious than the claim that global changes have been demonstrated. (LLM, conf=0.84)
boosteddirect- Asserted: passes — The authors put it forward as true.
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- 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
“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 Discussion reports smoking-associated hypomethylation of CYP1A1 in placenta, supporting that gene’s inclusion. But it explicitly says CYP1A1 and its promoter were not assayed in fetal blood; this paper does not establish cord-blood methylation changes in CYP1A1 or the other listed genes. (LLM, conf=0.88)
- 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 report smoking-associated cord-blood methylation differences in CYP1A1, AHRR, and GFI1—the likely intended gene behind “GF1.” The paper does not report a corresponding finding for FOXP3, so it does not support the full gene list attributed to it. (LLM, conf=0.88)
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
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In the paper
“Novakovic and colleagues 76 recently demonstrated persistent AHRR hypomethylation in blood monocytes at 1 year of age, and a separate longitudinal study detected persistent changes at 7 years of age.72,77”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Epigenetic Effects of Tobacco Smoke Exposure
What the sources say
- Could not verifycites [72] Suter, 2010, In utero tobacco exposure epigenetically modifies placental CYP1A1 expression, Metabolism sourceExperimental — accuracy not yet measured
The Results and Discussion describe CYP1A1 methylation in placenta and speculate that it may provide a memory of fetal tobacco exposure. Our copy does not report AHRR methylation or a longitudinal finding at age 7 (searched for AHRR and seven-year follow-up); no page numbers are available in the copy. (LLM, conf=0.76)
- Supportedcites [77] Richmond, 2015, Prenatal exposure to maternal smoking and offspring DNA methylation across the lifecourse: findings from the Avon Longitudinal Study of Parents and Children (ALSPAC), Hum Mol Genet source
The Results section (page not provided) reports longitudinal AHRR methylation measurements through age 7 in offspring exposed to maternal smoking. It describes partial methylation ‘catchup’ by that age, rather than complete disappearance of the smoking-associated difference. (LLM, conf=0.85)
boostedcorrelational- 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.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“These epigenetic changes in AHRR methylation persist well into postnatal life.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Epigenetic Effects of Tobacco Smoke Exposure
What the sources say
- Supportedcites [76] Novakovic, 2014, Postnatal stability, tissue, and time specific effects of AHRR methylation change in response to maternal smoking in pregnancy, Epigenetics source
The section “Maternal smoking-induced hypomethylation of AHRR is maintained at 18 mo” reports that the methylation difference remained significant in blood at 18 months. This supports persistence into postnatal life; the study did not assess persistence beyond 18 months. Page numbers are not provided in our copy. (LLM, conf=0.93)
- Could not verifycites [72] Suter, 2010, In utero tobacco exposure epigenetically modifies placental CYP1A1 expression, Metabolism sourceExperimental — accuracy not yet measured
The Introduction reports altered CYP1A1 methylation in placentas, while the Discussion describes persistence of tobacco-related epigenetic changes as a possibility, not an observed postnatal result. Searches for AHRR and postnatal persistence found no passage establishing that AHRR methylation changes persist after birth. Page numbers were not available in our copy. (LLM, conf=0.78)
- Supportedcites [77] Richmond, 2015, Prenatal exposure to maternal smoking and offspring DNA methylation across the lifecourse: findings from the Avon Longitudinal Study of Parents and Children (ALSPAC), Hum Mol Genet source
The Discussion states that AHRR showed a persistently perturbed methylation pattern after prenatal exposure to maternal smoking. The Results track AHRR methylation from birth through ages 7 and 17, supporting persistence well into postnatal life. (LLM, conf=0.94)
boosted- Asserted: passes — The authors put it forward as true.
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- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In addition, decreased expression of interferon-inducible GTPases and type 1 interferon response pathway genes induced by viral double-stranded RNA were found in the lungs of neonatal mice exposed to SHS. 33”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > SHS and Pulmonary Immune Responses
What the sources say
- Supportedcites [33] McGrath-Morrow, 2008, Impaired lung homeostasis in neonatal mice exposed to cigarette smoke, Am J Respir Cell Mol Biol source
The sections “CS Inhibited Interferon-Inducible GTPase Expression in Neonatal Lung” and “CS Inhibited Expression of Genes Activated by Double-Stranded (ds) RNA in Neonatal Lung” report reduced expression of both gene groups in smoke-exposed neonatal mouse lungs. The paper describes the latter genes as activated by viral dsRNA; it does not claim the mice were exposed to viral dsRNA. (LLM, conf=0.92)
plaindirect- Asserted: passes — The authors put it forward as true.
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- 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
“These neonatal changes correlated with maternal levels of cotinine.74”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Epigenetic Effects of Tobacco Smoke Exposure
What the sources say
- Supportedcites [74] Joubert, 2012, 450K epigenome-wide scan identifies differential DNA methylation in newborns related to maternal smoking during pregnancy, Environ Health Perspect source
The Results report that newborn AHRR methylation at cg05575921 decreased as maternal cotinine increased, with a statistically significant dose-dependent trend. The Discussion likewise describes a dose-dependent association between maternal smoking assessed by cotinine and lower AHRR methylation in cord blood. (LLM, conf=0.94)
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.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Neonatal mice exposed to nicotine in utero had enhanced M2 phenotype in their alveolar macrophages.65”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > SHS and Pulmonary Immune Responses
What the sources say
- Supportedcites [65] Wongtrakool, 2012, In utero nicotine exposure promotes M2 activation in neonatal mouse alveolar macrophages, Pediatr Res source
The Abstract Results report increased markers of alternative activation in alveolar macrophages from nicotine-exposed neonatal mice. The Discussion states that in utero nicotine exposure skewed the resting state of neonatal alveolar macrophages toward M2 activation. (LLM, conf=0.94)
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.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Indeed, in a 2013 study comparing neonates born to smoking and nonsmoking mothers, Almanzar and colleagues 64 found no difference in lymphocyte subsets between the two groups.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > SHS and Pulmonary Immune Responses
What the sources say
- Supportedcites [64] Almanzar, 2013, Maternal cigarette smoking and its effect on neonatal lymphocyte subpopulations and replication, BMC Pediatr source
The Results section reports no significant differences in the proportions of lymphocyte subpopulations between newborns of smoking and nonsmoking mothers. The Discussion states the same finding. The claim concerns lymphocyte subsets, not absolute lymphocyte counts. (LLM, conf=0.94)
plain- Asserted: passes — The authors put it forward as true.
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- 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
“Novakovic and colleagues 76 recently demonstrated persistent AHRR hypomethylation in blood monocytes at 1 year of age, and a separate longitudinal study detected persistent changes at 7 years of age.72,77”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Epigenetic Effects of Tobacco Smoke Exposure
What the sources say
- Partly supportedcites [76] Novakovic, 2014, Postnatal stability, tissue, and time specific effects of AHRR methylation change in response to maternal smoking in pregnancy, Epigenetics sourceExperimental — accuracy not yet measured
The section “Maternal smoking-induced hypomethylation of AHRR is maintained at 18 mo” reports that the methylation difference associated with maternal smoking persisted after birth. It measured peripheral blood mononuclear cells at 18 months, not isolated monocytes at 1 year of age. (LLM, conf=0.88)
boosted- 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
“Subsequent research has demonstrated physiologic changes, including increased airway resistance and decreased lung function after in utero smoke exposure in children with GSTTI and GSTP1 alleles.86,88”
§ 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 [86] Murdzoska, 2010, In utero smoke exposure and role of maternal and infant glutathione s-transferase genes on airway responsiveness and lung function in infancy, Am J Respir Crit Care Med source
- Partly supportedcites [88] Kabesch, 2004, Glutathione S transferase deficiency and passive smoking increase childhood asthma, Thorax sourceExperimental — accuracy not yet measured
The Results (page not provided) report decreased lung-function measurements in children with a GSTT1 null genotype exposed to smoke in utero. The paper studied GSTM1 and GSTT1, not GSTP1, and the cited passages do not report increased airway resistance. (LLM, conf=0.89)
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.
- Rests on an assumption: Glutathione S-transferase enzymes play a role in metabolizing tobacco products and reactive oxygen species.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“| Y N-myc expression | Nicotine caused fibroblast differentiation in nonhuman | 29 |”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Gaps in Knowledge and Future Directions
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 Methods (In Vitro differentiation; page unavailable) say that a directed protocol differentiated nonhuman primate embryonic stem cells into fibroblasts, with nicotine added to one experimental group. The Discussion reports altered gene expression in cells differentiated in nicotine’s presence, but the paper does not show that nicotine itself caused fibroblast differentiation. (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.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In this nested case control study, grandmaternal smoking was associated with a 2.1 OR risk of developing childhood asthma; however, this effect was unable to be replicated using data from the Avon Longitudinal Study of Parents and Children.83”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Epigenetic Effects of Tobacco Smoke Exposure
What the sources say
- Supportedcites [83] Miller, 2014, Do grandmaternal smoking patterns influence the etiology of childhood asthma?, Chest source
The Discussion explicitly says the authors failed to replicate the previously reported association between maternal prenatal smoking exposure and childhood respiratory outcomes. The Methods identify ALSPAC as the data source. The failure to replicate concerns the maternal-grandmother pathway; the paper reports a separate, suggestive paternal-grandmother association. (LLM, conf=0.93)
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.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The Norwegian Mother and Child Cohort Study also found a strong association between grandmaternal smoking during pregnancy and childhood asthma.84”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Epigenetic Effects of Tobacco Smoke Exposure
What the sources say
- Partly supportedcites [84] Magnus, 2015, Grandmother's smoking when pregnant with the mother and asthma in the grandchild: the Norwegian Mother and Child Cohort Study, Thorax sourceExperimental — accuracy not yet measured
The Results report an association between the grandmother’s smoking while pregnant with the mother and asthma in the grandchild, but explicitly call it “modest” (adjusted risk ratios 1.15–1.21). Describing the association as strong overstates the finding. (LLM, conf=0.91)
boostedcorrelational- 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
Every source the paper cites for this claim was checked and supports it.
In the paper
“Furthermore, they reported that the lungs of mice exposed to nicotine-containing e-cigarette aerosols had decreased total glutathione.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Electronic Cigarettes and Lung Development
What the sources say
- Supportedcites [95] Lerner, 2015, Vapors produced by electronic cigarettes and e-juices with flavorings induce toxicity, oxidative stress, and inflammatory response in lung epithelial cells and in mouse lung, PLoS One source
The Materials and Methods section (‘E-cigarette aerosol mouse exposure’) specifies that the mice inhaled aerosols generated from e-cigarettes containing 16 mg nicotine. The Results section (‘Intracellular glutathione levels in mouse lung exposed to short-term chronic e-cigarette aerosols’) reports lower total glutathione in exposed mouse lungs than in air-exposed controls. (LLM, conf=0.94)
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.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“One of the first articles looking at the effects of in utero smoke exposure on fetal lung-specific methylation found changes in methylation of DPP10, a gene associated with asthma.22”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Epigenetic Effects of Tobacco Smoke Exposure
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 that DPP10 was among the most significant genes with differential methylation in fetal lung tissue associated with in utero nicotine exposure, used as a surrogate for smoke exposure. The Discussion identifies DPP10 as a gene associated with asthma and describes this as early work on methylation in developing human fetal lung tissue. (LLM, conf=0.92)
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.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“| [ a7 nAChRs | Prenatal nicotine exposure caused [ a7 nAChRs in airway, | 30 |”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Gaps in Knowledge and Future Directions
What the sources say
- Partly supportedcites [30] Sekhon, 1999, Prenatal nicotine increases pulmonary alpha7 nicotinic receptor expression and alters fetal lung development in monkeys, J Clin Invest sourceExperimental — accuracy not yet measured
The Nicotinic receptor immunohistochemistry section reports that prenatal nicotine markedly increased α7 staining in airway epithelial cells, cartilaginous airway wall regions, and blood vessel walls. Figure 2 (p. 640) also shows α7 staining in control fetuses, so the paper supports increased expression, not the claim that nicotine caused the receptors to appear. It does not establish increased expression in cartilage itself. (LLM, conf=0.84)
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.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Taken together, these findings indicate that exposure to e-cigarette aerosols may increase oxidative stress and inflammation in the lung.95”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Electronic Cigarettes and Lung Development
What the sources say
- Supportedcites [95] Lerner, 2015, Vapors produced by electronic cigarettes and e-juices with flavorings induce toxicity, oxidative stress, and inflammatory response in lung epithelial cells and in mouse lung, PLoS One source
The Results sections report reduced glutathione levels in mouse lungs after e-cigarette aerosol exposure and increased inflammatory mediators in bronchoalveolar lavage fluid. The Discussion says inhaling the aerosols could impose oxidative stress, matching the claim’s cautious wording. Page numbers are unavailable in our copy. (LLM, conf=0.93)
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.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The first genomewide interaction study of early life tobacco exposure and asthma was published in 2014 and identified novel polymorphisms on chromosomes 6 and 18. 85”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Gene-Environment Interactions and Tobacco Smoke Exposure
What the sources say
- Supportedcites [85] Scholtens, 2014, Novel childhood asthma genes interact with in utero and early-life tobacco smoke exposure, J Allergy Clin Immunol source
The main text calls this the first hypothesis-free genome-wide interaction study of childhood asthma and tobacco-smoke exposure. It reports previously unidentified SNPs on chromosome 18 near EPB41L3 and chromosome 6 in PACRG, while describing the interaction evidence as suggestive rather than genome-wide significant. (LLM, conf=0.90)
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.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“| Y Interferon-g | Prenatal smoke exposure caused Th1 and Th2 changes in | 31 |”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Gaps in Knowledge and Future Directions
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 Results section reports that, after Aspergillus fumigatus sensitization, prenatally secondhand-smoke-exposed mice had increased Th2 cytokines IL-4 and IL-13. Another Results passage reports reduced allergen-induced T-bet expression and failure to upregulate the Th1 cytokine IFN-γ after Aspergillus challenge. The copy provides no page numbers for these passages. (LLM, conf=0.93)
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.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Additional candidate genes, CYP1A1, ADAM33, and TNF, have been suggested to modify the risk of subsequent asthma.85,90,91”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Gene-Environment Interactions and Tobacco Smoke Exposure
What the sources say
- Partly supportedcites [85] Scholtens, 2014, Novel childhood asthma genes interact with in utero and early-life tobacco smoke exposure, J Allergy Clin Immunol sourceExperimental — accuracy not yet measured
In the paper’s discussion (page not available in our copy), TNF and ADAM33 are described as genes previously reported to interact with tobacco-smoke exposure in asthma development. CYP1A1 is not mentioned, and TNF and ADAM33 were not among this study’s most significant hits. The source therefore supports the suggestion for two of the three named genes, not all three. (LLM, conf=0.86)
- Not checked — no full text of the sourcecites [90] Chen, 2011, Maternal smoking during pregnancy, polymorphic CYP1A1 and GSTM1, and lung-function measures in urban family children, Environ Res source
- Not checked — no full text of the sourcecites [91] Reijmerink, 2009, Smoke exposure interacts with ADAM33 polymorphisms in the development of lung function and hyperresponsiveness, Allergy source
hedgedcorrelational- 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
“Lerner and colleagues 95 reported increased levels of the proinflammatory cytokines, IL-6, and IL-8 in human epithelial cells and fibroblasts exposed to nicotine and nonnicotine flavored e-cigarette juices.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Electronic Cigarettes and Lung Development
What the sources say
- Partly supportedcites [95] Lerner, 2015, Vapors produced by electronic cigarettes and e-juices with flavorings induce toxicity, oxidative stress, and inflammatory response in lung epithelial cells and in mouse lung, PLoS One sourceExperimental — accuracy not yet measured
The Results report increased IL-6 and IL-8 secretion in human H292 epithelial cells exposed to tobacco-flavored e-cigarette aerosols. In the lung-fibroblast Results, only cinnamon-flavored e-liquid significantly increased IL-8 versus controls; the passage does not report increased IL-6 in fibroblasts, and nicotine-containing tobacco e-liquid did not significantly increase fibroblast IL-8 versus controls. Page numbers were not provided in our copy's passages. (LLM, conf=0.88)
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.
- Partly supported
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
“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.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Abstract
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.
- Rests on an assumption: Observed associations between tobacco smoke exposure and childhood respiratory outcomes reflect causal effects of tobacco smoke or nicotine.
- Rests on an assumption: Nicotine is a key mediator of the adverse effects of tobacco smoke on lung development.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Exposed neonates are at increased risk for diminished lung function, altered central and peripheral respiratory chemoreception, and increased asthma symptoms throughout childhood.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Abstract
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.
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
“Nicotine has also been shown to be concentrated in the breast milk of mothers who smoke.13,14”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Abstract
What the sources say
- Not checked — no full text of the sourcecites [13] Schulte-Hobein, 1992, Cigarette smoke exposure and development of infants throughout the first year of life: influence of passive smoking and nursing on cotinine levels in breast milk and infant's urine, Acta Paediatr source
- Not checked — no full text of the sourcecites [14] Schwartz-Bickenbach, 1987, Smoking and passive smoking during pregnancy and early infancy: effects on birth weight, lactation period, and cotinine concentrations in mother's milk and infant's urine, Toxicol Lett 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.
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
“Indeed, cotinine levels in neonates exposed to in utero tobacco smoke have been reported to be similar to that of active smoking adults.24,25”
§ 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 [24] Ivorra, 2014, High cotinine levels are persistent during the first days of life in newborn second hand smokers, Drug Alcohol Depend source
- Not checked — no full text of the sourcecites [25] Chazeron, 2008, GC-MS determined cotinine in an epidemiological study on smoking status at delivery, Pulm Pharmacol Ther source
hedged- 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.
In the paper
“Postnatal exposure of children to SHS continues to be widespread.”
§ 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: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
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
“Nicotine, the primary addictive substance in tobacco smoke, has been shown to cross the placenta in utero as evidenced by high levels of cotinine, a nicotine metabolite, in the amniotic fluid of pregnant smokers and in blood spots from neonates exposed in utero.11,12”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Abstract
What the sources say
- Not checked — no full text of the sourcecites [11] Luck, 1985, Extent of nicotine and cotinine transfer to the human fetus, placenta and amniotic fluid of smoking mothers, Dev Pharmacol Ther source
- Not checked — no full text of the sourcecites [12] Jauniaux, 1999, Maternal tobacco exposure and cotinine levels in fetal fluids in the first half of pregnancy, Obstet Gynecol source
boosteddirect- Asserted: passes — The authors put it forward as true.
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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
“Furthermore, infants and young children may be at highest risk for toxicity from secondhand and thirdhand smoke exposure because they tend to spend more time indoors, have faster respiratory rates, have a greater relative body surface area, and have more hand or oral behaviors than do older children.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Abstract
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Exposed neonates are at increased risk for diminished lung function, altered central and peripheral respiratory chemoreception, and increased asthma symptoms throughout childhood.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Abstract
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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
plaincorrelational- Asserted: passes — The authors put it forward as true.
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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
“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.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
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- Rests on an assumption: Observed associations between tobacco smoke exposure and childhood respiratory outcomes reflect causal effects of tobacco smoke or nicotine.
- Rests on an assumption: Nicotine is a key mediator of the adverse effects of tobacco smoke on lung development.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Exposed neonates are at increased risk for diminished lung function, altered central and peripheral respiratory chemoreception, and increased asthma symptoms throughout childhood.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Abstract
plaincorrelational- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“Tobacco smoke exposure during prenatal and postnatal lung development is associated with an increase in respiratory morbidities during childhood.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Abstract
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Rests on an assumption: Observed associations between tobacco smoke exposure and childhood respiratory outcomes reflect causal effects of tobacco smoke or nicotine.
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
“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.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Rests on an assumption: Observed associations between tobacco smoke exposure and childhood respiratory outcomes reflect causal effects of tobacco smoke or nicotine.
- Rests on an assumption: Nicotine is a key mediator of the adverse effects of tobacco smoke on lung development.
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
“This finding suggests that that the risk of COPD in adult life may be influenced by SHS during childhood because children exposed to SHS are more likely to have a history of lower respiratory tract infections.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Abstract
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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
“Because of oxidation and breakdown processes, thirdhand smoke may have enhanced toxicity compared with mainstream smoke.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Abstract
hedgedconditional- Asserted: passes — The authors put it forward as true.
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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
“Aberrant growth and inflammation of the small airways from tobacco exposure during in utero and early postnatal life may, in part, account for the observed symptoms and outcomes in these studies.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > SHS and Lung Function in Children
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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
“nAChRs have been shown to be expressed in the brain and lung during early fetal life, thus representing a potential mechanism for the effects of nicotine on development.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Normal Lung Development
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- Rests on an assumption: Nicotine is a key mediator of the adverse effects of tobacco smoke on lung development.
In the paper
“Human lung development spans both prenatal and postnatal life 1 and can be adversely affected by exposure to tobacco smoke and nicotine during both of these periods.”
§ 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 [1] Smith, 2010, Normal development of the lung and premature birth, Paediatr Respir Rev source
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“A study in neonatal rats found that pups exposed to prenatal cigarette smoke had prolonged gasping following a hyperthermic or hypoxic exposure.48”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Maternal Smoking and Sudden Infant Death Syndrome
What the sources say
- Not checked — no full text of the sourcecites [48] Pendlebury, 2008, Respiratory control in neonatal rats exposed to prenatal cigarette smoke, Am J Respir Crit Care Med source
plaindirect- Asserted: passes — The authors put it forward as true.
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“nAChRs have been shown to be expressed in the brain and lung during early fetal life, thus representing a potential mechanism for the effects of nicotine on development.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Normal Lung Development
boosted- Asserted: passes — The authors put it forward as true.
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In the paper
“Mitchell and Milerad 45 reported that the pooled relative risk of SIDS associated with maternal smoking was 2.86; furthermore, if a causal association was assumed, one-third of SIDS deaths may have been avoided if the infant had not been exposed to smoke in utero.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Maternal Smoking and Sudden Infant Death Syndrome
What the sources say
- Not checked — no full text of the sourcecites [45] Mitchell, 2006, Smoking and the sudden infant death syndrome, Rev Environ Health source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- 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
“A Finnish study that examined young children with a history of multitrigger wheezing found that children of mothers who smoked, validated by cotinine levels, were more likely to have increased airway resistance and higher fraction of exhaled nitric oxide levels than were nonexposed children.17”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > SHS and Lung Function in Children
What the sources say
- 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
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Human bronchial and endothelial cells have been reported to express a3/b4 and a7 nAChRs.35”
§ 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 [35] Wang, 2001, Human bronchial epithelial and endothelial cells express alpha7 nicotinic acetylcholine receptors, Mol Pharmacol source
hedged- Asserted: passes — The authors put it forward as true.
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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 3-yearold children within the Generation R cohort, there was an increased risk of wheezing with any prenatal or postnatal tobacco smoke exposure, but at 4 years of age, those with postnatal exposure alone did not have increased wheezing.5,50”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > SHS and Lung Function in Children
What the sources say
- Not checked — no full text of the sourcecites [5] den Dekker, 2015, Tobacco smoke exposure, airway resistance, and asthma in school-age children: the Generation R Study, Chest source
- Not checked — no full text of the sourcecites [50] Duijts, 2012, Fetal exposure to maternal and paternal smoking and the risks of wheezing in preschool children: the Generation R Study, Chest source
plain- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“Tobacco smoke exposure has been linked to an increased risk of sudden infant death syndrome (SIDS).”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Maternal Smoking and Sudden Infant Death Syndrome
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Proskocil and colleagues 42 reported that vitamin C, when given to pregnant rhesus monkeys, improved lung function in nicotine-exposed offspring.”
§ 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 [42] Proskocil, 2005, Vitamin C prevents the effects of prenatal nicotine on pulmonary function in newborn monkeys, Am J Respir Crit Care Med source
plaindirect- Asserted: passes — The authors put it forward as true.
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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 3-yearold children within the Generation R cohort, there was an increased risk of wheezing with any prenatal or postnatal tobacco smoke exposure, but at 4 years of age, those with postnatal exposure alone did not have increased wheezing.5,50”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > SHS and Lung Function in Children
What the sources say
- Not checked — no full text of the sourcecites [5] den Dekker, 2015, Tobacco smoke exposure, airway resistance, and asthma in school-age children: the Generation R Study, Chest source
- Not checked — no full text of the sourcecites [50] Duijts, 2012, Fetal exposure to maternal and paternal smoking and the risks of wheezing in preschool children: the Generation R Study, Chest 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.
In the paper
“Mitchell and Milerad 45 reported that the pooled relative risk of SIDS associated with maternal smoking was 2.86; furthermore, if a causal association was assumed, one-third of SIDS deaths may have been avoided if the infant had not been exposed to smoke in utero.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Maternal Smoking and Sudden Infant Death Syndrome
What the sources say
- Not checked — no full text of the sourcecites [45] Mitchell, 2006, Smoking and the sudden infant death syndrome, Rev Environ Health source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Noakes and colleagues 63 found that cord blood from neonates exposed to smoke in utero had increased levels of IL-13 after antigen challenge.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > SHS and Pulmonary Immune Responses
What the sources say
- Not checked — no full text of the sourcecites [63] Noakes, 2003, Maternal smoking in pregnancy alters neonatal cytokine responses, Allergy source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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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
“Prenatal exposure to tobacco smoke can cause decreased levels of cord blood interferon-g, and continued environmental tobacco smoke exposure has been shown to suppress interferon-g levels through 11 years of age.59,61”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > SHS and Pulmonary Immune Responses
What the sources say
- Not checked — no full text of the sourcecites [59] Macaubas, 2003, Association between antenatal cytokine production and the development of atopy and asthma at age 6 years, Lancet source
- Not checked — no full text of the sourcecites [61] Tebow, 2008, Effects of parental smoking on interferon gamma production in children, Pediatrics source
plaindirect- Asserted: passes — The authors put it forward as true.
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“After birth, the immune response normally shifts toward a Th1 immune response.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > SHS and Pulmonary Immune Responses
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“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”
§ 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 [79] Armstrong, 2014, Global and gene-specific DNA methylation across multiple tissues in early infancy: implications for children's health research, FASEB J source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Consequently, fetal T-helper cells exhibit a predominantly antiinflammatory Th2 response.60”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > SHS and Pulmonary Immune Responses
What the sources say
- Not checked — no full text of the sourcecites [60] Ygberg, 2012, The developing immune system - from foetus to toddler, Acta Paediatr source
plain- Asserted: passes — The authors put it forward as true.
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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
“Prenatal exposure to tobacco smoke can cause decreased levels of cord blood interferon-g, and continued environmental tobacco smoke exposure has been shown to suppress interferon-g levels through 11 years of age.59,61”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > SHS and Pulmonary Immune Responses
What the sources say
- Not checked — no full text of the sourcecites [59] Macaubas, 2003, Association between antenatal cytokine production and the development of atopy and asthma at age 6 years, Lancet source
- Not checked — no full text of the sourcecites [61] Tebow, 2008, Effects of parental smoking on interferon gamma production in children, Pediatrics source
plaindirect- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“In addition to decreasing interferon-g levels, in utero smoke increases the levels of cytokines associated with Th2 immune profiles.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > SHS and Pulmonary Immune Responses
plaindirect- Asserted: passes — The authors put it forward as true.
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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
“Changes in AHRR methylation may contribute to altered detoxification function and subsequent disease development.”
§ 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.
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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.
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None of the sources cited for this claim have been checked yet.
In the paper
“Studies of human cord blood have shown decreased methylation in AHRR loci in neonates similar to immune cell methylation patterns in adult smokers.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Epigenetic Effects of Tobacco Smoke Exposure
plaincorrelational- Asserted: passes — The authors put it forward as true.
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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
“Prenatal maternal smoking may carry a higher risk of subsequent infection, suggesting a developmental mechanism for the increased vulnerability, 58,59 but the underlying mechanisms that account for this increased infection risk are not fully understood.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > SHS Exposure and Childhood Respiratory Infections
What the sources say
- Not checked — no full text of the sourcecites [58] Haberg, 2007, Effects of pre- and postnatal exposure to parental smoking on early childhood respiratory health, Am J Epidemiol source
- Not checked — no full text of the sourcecites [59] Macaubas, 2003, Association between antenatal cytokine production and the development of atopy and asthma at age 6 years, Lancet source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- Based: passes — The paper gives a reason why it holds.
In the paper
“In this nested case control study, grandmaternal smoking was associated with a 2.1 OR risk of developing childhood asthma; however, this effect was unable to be replicated using data from the Avon Longitudinal Study of Parents and Children.83”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Epigenetic Effects of Tobacco Smoke Exposure
What the sources say
- Not matchedcites [82] Li, 2005, Maternal and grandmaternal smoking patterns are associated with early childhood asthma, Chest
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Not matched
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
“This in turn may cause different physiologic or pathologic changes in the developing lung compared with those seen with nicotine replacement therapy.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Electronic Cigarettes and Lung Development
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.
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- Rests on an assumption: Electronic nicotine delivery systems have the capacity to deliver a high level burst of nicotine.
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
“Intriguingly, the epigenetic effects of tobacco smoke may extend beyond direct effects on gene expression to transgenerational changes in lung development.”
§ 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.
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In the paper
“Wu and colleagues 89 reported in a population-based birth cohort that maternal smoking increased the risk of wheezing in children who had a GSTP1 AA genotype; however, the effect of maternal smoking on wheeze diminished with age.”
§ 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 [89] Wu, 2013, Interaction between glutathione S-transferase variants, maternal smoking and childhood wheezing changes with age, Pediatr Allergy Immunol 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.
In the paper
“Wu and colleagues 89 reported in a population-based birth cohort that maternal smoking increased the risk of wheezing in children who had a GSTP1 AA genotype; however, the effect of maternal smoking on wheeze diminished with age.”
§ 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 [89] Wu, 2013, Interaction between glutathione S-transferase variants, maternal smoking and childhood wheezing changes with age, Pediatr Allergy Immunol 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.
In the paper
“One study reported that non-e-cigarette users exposed to e-cigarette aerosols in the environment had similar cotinine levels as those exposed to SHS from tobacco-containing cigarettes.92”
§ 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 [92] Ballbe, 2014, Cigarettes vs. e-cigarettes: passive exposure at home measured by means of airborne marker and biomarkers, Environ Res source
plain- Asserted: passes — The authors put it forward as true.
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- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Linkage studies have also implicated chromosomal regions 1p, 1q, 5q, and 17p as modifying asthma risk after early life smoke exposure.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Gene-Environment Interactions and Tobacco Smoke Exposure
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Based: passes — The paper gives a reason why it holds.
In the paper
“Polymorphisms have been implicated in asthma pathogenesis.86”
§ 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 [86] Murdzoska, 2010, In utero smoke exposure and role of maternal and infant glutathione s-transferase genes on airway responsiveness and lung function in infancy, 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: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
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
“Although data are limited regarding the pulmonary effects of e-cigarette aerosols on fetal development, the nicotine component of these aerosols may have developmental consequences similar to those of other forms of nicotine delivery.”
§ Impact of Tobacco Smoke and Nicotine Exposure on Lung Development > Electronic Cigarettes and Lung Development
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. 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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