Chronic maternal nicotine exposure during gestation and lactation and the development of the lung parenchyma in the offspring

Maritz, Gert S.; Windvogel, Shantal Lynn

doi:10.1016/j.pathophys.2003.10.001

Cited by 26 publications

(25 citation statements)

References 27 publications

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“…The lung, during its long process of maturation from the embryonic phase of development in utero up to adolescence, is highly susceptible to damage caused by exposure to environmental toxicants, and particularly to tobacco smoke in pregnancy [32-34]. …”

Section: Discussionmentioning

confidence: 99%

Possible role of the α7 nicotinic receptors in mediating nicotine’s effect on developing lung – implications in unexplained human perinatal death

et al. 2014

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BackgroundIt is well known that maternal smoking during pregnancy is very harmful to the fetus. Prenatal nicotine absorption, in particular, is associated with alterations in lung development and functions at birth and with respiratory disorders in infancy. Many of the pulmonary disorders are mediated by the interaction of nicotine with the nicotinic receptors (nAChRs), above all with the α7 nAChR subunits that are widely expressed in the developing lung. To determine whether the lung hypoplasia frequently observed in victims of sudden fetal and neonatal death with a smoker mother may result from nicotine interacting with lung nicotinic receptors, we investigated by immunohistochemistry the possible presence of the α7 nAChR subunit overexpression in these pathologies.MethodsIn lung histological sections from 45 subjects who died of sudden intrauterine unexplained death syndrome (SIUDS) and 15 subjects who died of sudden infant death syndrome (SIDS), we applied the radial alveolar count (RAC) to evaluate the degree of lung maturation, and the immunohistochemical technique for nAChRs, in particular for the α7 nAChR subunit identification. In the same cases, an in-depth study of the autonomic nervous system was performed to highlight possible developmental alterations of the main vital centers located in the brainstem.ResultsWe diagnosed a “lung hypoplasia”, on the basis of RAC values lower than the normal reference values, in 63% of SIUDS/SIDS cases and 8% of controls. In addition, we observed a significantly higher incidence of strong α7 nAChR immunostaining in lung epithelial cells and lung vessel walls in sudden fetal and infant death cases with a smoker mother than in age-matched controls. Hypoplasia of the raphe, the parafacial, the Kölliker-Fuse, the arcuate and the pre-Bötzinger nuclei was at the same time present in the brainstem of these victims.ConclusionsThese findings demonstrate that when crossing the placenta, nicotine can interact with nicotinic receptors of both neuronal and non-neuronal cells, leading to lung and nervous system defective development, respectively. This work stresses the importance of implementing preventable measures to decrease the noxious potential of nicotine in pregnancy.

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Section: Discussionmentioning

confidence: 99%

Possible role of the α7 nicotinic receptors in mediating nicotine’s effect on developing lung – implications in unexplained human perinatal death

et al. 2014

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“…For instance, nicotine can alter airway structure and mechanics in fetal monkeys, resulting in decreased pulmonary function parameters such as forced expiratory volume, forced vital capacity, and expiratory reserve volume (Sekhon et al , 1999, 2001, 2002). In addition, nicotine impairs alveolarization in the lungs of perinatally exposed rats (Maritz, 2002; Maritz and Thomas, 1994; Maritz and Windvogel, 2003; Petre et al , 2008). Offspring of nicotine-treated lambs also had abnormal postnatal breathing patterns (Hafstrom et al , 2002a) and proximal airway obstruction (Sandberg et al , 2004).…”

Section: Long-term Effects Of Fetal and Neonatal Exposure To Nicotinementioning

confidence: 99%

Long-Term Consequences of Fetal and Neonatal Nicotine Exposure: A Critical Review

Bruin¹,

Gerstein

Holloway³

2010

Toxicological Sciences

322

269

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Cigarette smoking during pregnancy is associated with numerous obstetrical, fetal, and developmental complications, as well as an increased risk of adverse health consequences in the adult offspring. Nicotine replacement therapy (NRT) has been developed as a pharmacotherapy for smoking cessation and is considered to be a safer alternative for women to smoking during pregnancy. The safety of NRT use during pregnancy has been evaluated in a limited number of short-term human trials, but there is currently no information on the long-term effects of developmental nicotine exposure in humans. However, animal studies suggest that nicotine alone may be a key chemical responsible for many of the long-term effects associated with maternal cigarette smoking on the offspring, such as impaired fertility, type 2 diabetes, obesity, hypertension, neurobehavioral defects, and respiratory dysfunction. This review will examine the long-term effects of fetal and neonatal nicotine exposure on postnatal health.

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“…Studies in monkeys (Sekhon et al, 1999) have clearly showed that nicotine exposure during pregnancy increases the development of a 7 nicotinic receptors in cells implicated in lung development. Pulmonary hypoplasia and other abnormalities in pulmonary and bronchial development were found in the offspring of experimental animals after exposure to nicotine during gestation (Sekhon et al, 1999;Maritz, 1987Maritz, , 1997Maritz et al, 2003aMaritz et al, ,b, 2005. It is also suggested that maternal nicotine exposure suppresses lysyl oxidase activity and in this way contributes to the gradual deterioration of the lung parenchyma of the offspring.…”

Section: Nicotine Replacement Therapymentioning

confidence: 99%

Nicotine and lung development

Maritz

2008

Birth Defects Research Pt C

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Nicotine is found in tobacco smoke. It is a habit forming substance and is prescribed by health professionals to assist smokers to quit smoking. It is rapidly absorbed from the lungs of smokers. It crosses the placenta and accumulates in the developing fetus. Nicotine induces formation of oxygen radicals and at the same time also reduces the antioxidant capacity of the lungs. Nicotine and the oxidants cause point mutations in the DNA molecule, thereby changing the program that controls lung growth and maintenance of lung structure. The data available indicate that maternal nicotine exposure induces a persistent inhibition of glycolysis and a drastically increased cAMP level. These metabolic changes are thought to contribute to the faster aging of the lungs of the offspring of mothers that are exposed to nicotine via the placenta and mother's milk. The lungs of these animals are more susceptible to damage as shown by the gradual deterioration of the lung parenchyma. The rapid metabolic and structural aging of the lungs of the animals that were exposed to nicotine via the placenta and mother's milk, and thus during phases of lung development characterized by rapid cell division, is likely due to "programming" induced by nicotine. It is, therefore, not advisable to use nicotine during gestation and lactation.

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Chronic maternal nicotine exposure during gestation and lactation and the development of the lung parenchyma in the offspring

Cited by 26 publications

References 27 publications

Possible role of the α7 nicotinic receptors in mediating nicotine’s effect on developing lung – implications in unexplained human perinatal death

Possible role of the α7 nicotinic receptors in mediating nicotine’s effect on developing lung – implications in unexplained human perinatal death

Long-Term Consequences of Fetal and Neonatal Nicotine Exposure: A Critical Review

Nicotine and lung development

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