Evidence map›Paper›PMID 22246862›Full record

ArticleAmerican journal of respiratory cell and molecular biology2012

Prenatal nicotine exposure alters lung function and airway geometry through α7 nicotinic receptors.

Cherry Wongtrakool, Ningshan Wang, Dallas M Hyde, Jesse Roman, Eliot R Spindel

Abstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

74 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Trial
  6. Article
  7. Review
  8. Article
  9. Single-Cell Multiome Impact of Prenatal Heavy Metal Exposure on Early Airway Development.American journal of respiratory cell and molecular biology · 2026
    Article
  10. Moderate-to-late prematurity: understanding respiratory consequences and modifiable risk factors.European respiratory review : an official journal of the European Respiratory Society · 2025
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Nicotinic receptors in airway disease.American journal of physiology. Lung cellular and molecular physiology · 2024
    Review
  16. Article
  17. Dysanapsis as a Determinant of Lung Function in Development and Disease.American journal of respiratory and critical care medicine · 2023
    Article
  18. Review
  19. Article
  20. Article

14 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Cherry WongtrakoolAtlanta VA Medical Center, 1670 Clairmont Road, Decatur, GA 30033, USA. cwongtr@emory.edu
Ningshan Wang
Dallas M Hyde
Jesse Roman
Eliot R Spindel

Funding

YR 50 PROJ- ROBERTS PRIMATE ISLETP51RR000163 · NCRR · OREGON REGIONAL PRIMATE RESEARCH CENTER · PI FRUH, KLAUS J · 1985 to 2011
$140.8M
Nicotine &Alpha7 nicotinic receptor in lung developmentR01HL066118 · NHLBI · OREGON HEALTH & SCIENCE UNIVERSITY · PI SPINDEL, ELIOT R · 2002 to 2006
$1.8M
Prenatal nicotine lung development &airway dysfunctionK08HL080293 · NHLBI · EMORY UNIVERSITY · PI WONGTRAKOOL, CHERRY P · 2005 to 2009
$629k
REPRODUCTIVE STEROIDS AND EXPERIMENTAL STROKEK01RR000163 · NCRR · OREGON HEALTH AND SCIENCE UNIVERSITY · PI MURPHY, STEPHANIE J · 2000 to 2004
$479k
NCRR NIH HHS K01 RR000163NCRR NIH HHS P51 RR000163NCRR NIH HHS RR00163NHLBI NIH HHS HL066118NHLBI NIH HHS HL080293NHLBI NIH HHS K08 HL080293NHLBI NIH HHS R01 HL066118
6 · The paper itself

Abstract

Maternal smoking during pregnancy has been associated with adverse effects on respiratory health. Whereas the epidemiologic link is incontrovertible, the mechanisms responsible for this association are still poorly understood. Although cigarette smoke has many toxic constituents, nicotine, the major addictive component in cigarette smoke, may play a more significant role than previously realized. The objectives of this study were to determine whether exposure to nicotine prenatally leads to alterations in pulmonary function and airway geometry in offspring, and whether α7 nicotinic acetylcholine receptors (nAChRs) mediate these effects. In a murine model of in utero nicotine exposure, pulmonary function, airway size and number, methacholine response, and collagen deposition were examined. Exposure periods included Gestation Days 7-21, Gestation Day 14 to Postnatal Day 7, and Postnatal Days 3-15. Prenatal nicotine exposure decreases forced expiratory flows in offspring through α7 nAChR-mediated signals, and the critical period of nicotine exposure was between Prenatal Day 14 and Postnatal Day 7. These physiologic changes were associated with increased airway length and decreased diameter. In addition, adult mice exposed to prenatal nicotine exhibit an increased response to methacholine challenge, even in the absence of allergic sensitization. Collagen expression was increased between adjacent airways and vessels, which was absent in α7 nAChR knockout mice. These observations provide a unified mechanism of how maternal smoking during pregnancy may lead to lifelong alterations in offspring pulmonary function and increased risk of asthma, and suggest potential targets to counteract those effects.

Indexed as

Maternal Exposurealpha7 Nicotinic Acetylcholine ReceptorAnimalsBronchiFemaleHumansLungMiceMice, KnockoutModels, AnimalNicotinePregnancyReceptors, Nicotinicalpha7 Nicotinic Acetylcholine ReceptorChrna7 protein, humanChrna7 protein, mouseNicotineReceptors, Nicotinic

Identifiers

PMID22246862
PMCPMC3359906

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.