Nicotine and cotinine concentrations in serum and milk of nursing smokers.

Luck, W. A. P.; Nau, Heinz

doi:10.1111/j.1365-2125.1984.tb05014.x

Cited by 147 publications

(91 citation statements)

References 26 publications

(43 reference statements)

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“…There are many agents in smoke that may be detrimental to the developing lung, but there is plenty of evidence to support direct alteration of fetal lung development by nicotine. Nicotine crosses the human placenta with minimal biotransformation (25), and it accumulates in fetal blood, maternal milk, and amniotic fluid, despite increased nicotine clearance during pregnancy, resulting in exposure of the fetus to even higher levels than the smoking mother (8,26,46). Nicotine accumulates in several fetal tissues, including the respiratory tract, suggesting that nicotine is the likely agent that alters lung development in the fetus of the pregnant smoker (46).…”

Section: Discussionmentioning

confidence: 99%

PPARγ agonist rosiglitazone prevents perinatal nicotine exposure-induced asthma in rat offspring

Liu

Sakurai

O'Roark

et al. 2011

American Journal of Physiology-Lung Cellular and Molecular Phys

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Kenyon NJ, Torday JS, Rehan VK. PPAR␥ agonist rosiglitazone prevents perinatal nicotine exposure-induced asthma in rat offspring. Am J Physiol Lung Cell Mol Physiol 300: L710 -L717, 2011. First published February 25, 2011 doi:10.1152/ajplung.00337.2010.-Perinatal exposure to maternal smoke is associated with adverse pulmonary effects, including reduced lung function and increased incidence of asthma. However, the mechanisms underlying these effects are unknown, and there is no effective preventive and/or therapeutic intervention. Recently, we suggested that downregulation of homeostatic mesenchymal peroxisome proliferator-activated receptor-␥ (PPAR␥) signaling following in utero nicotine exposure might contribute to chronic lung diseases such as asthma. We used an in vivo rat model to determine the effect of perinatal nicotine exposure on 1) offspring pulmonary function, 2) mesenchymal markers of airway contractility in trachea and lung tissue, and 3) whether administration of a PPAR␥ agonist, rosiglitazone (RGZ), blocks the molecular and functional effects of perinatal nicotine exposure on offspring lung. Pregnant SpragueDawley rat dams received placebo, nicotine, or nicotine ϩ RGZ daily from embryonic day 6 until postnatal day 21, when respiratory system resistance, compliance, tracheal contractility, and the expression of markers of pulmonary contractility were determined. A significant increase in resistance and a decrease in compliance under basal conditions, with more pronounced changes following methacholine challenge, were observed with perinatal nicotine exposure compared with control. Tracheal constriction response and expression of mesenchymal markers of airway contractility were also significantly increased following perinatal nicotine exposure. Concomitant treatment with RGZ completely blocked the nicotine-induced alterations in pulmonary function, as well as the markers of airway contractility, at proximal and distal airway levels. These data suggest that perinatal smoke exposure-induced asthma can be effectively blocked by PPAR␥ agonists.pregnancy; peroxisome proliferator-activated receptor-␥; smoke THERE IS STRONG EPIDEMIOLOGICAL and experimental evidence that perinatal exposure to maternal smoking results in detrimental long-term effects on lung growth and function, including significant suppression of alveolarization and increased predisposition to asthma in the offspring (2, 4 -6, 9, 13-15, 17, 27, 30, 42, 44, 45, 49). Since the mechanisms underlying these adverse pulmonary effects remain incompletely understood, there are no effective preventive or therapeutic interventions. Recently, on the basis of in vitro and in vivo studies from our laboratory, we suggested that downregulation of homeostatic lung mesenchymal peroxisome proliferator-activated receptor-␥ (PPAR␥) signaling might be a key contributor to chronic lung diseases such as bronchopulmonary dysplasia and asthma (23,34,36,37,48). We previously showed that in vitro and in vivo nicotine exposures result in the downregulation of pulmo...

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Section: Discussionmentioning

confidence: 99%

PPARγ agonist rosiglitazone prevents perinatal nicotine exposure-induced asthma in rat offspring

Liu

Sakurai

O'Roark

et al. 2011

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Due to the relatively high milk/plasma quotient of approximately 3, nicotine may even reach higher levels in milk than in the blood of the mother, whereas this quotient is much lower (0.78) for cotinine (37). Ekstroem and Gustavsson (38) found levels of up to 95 ng/mL nicotine in breast milk from smokers.…”

Section: Mycotoxinsmentioning

confidence: 99%

Nurturing and Breast-Feeding: Exposure to Chemicals in Breast Milk

Somogyi¹,

Beck²

1993

Environmental Health Perspectives

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All chemicals that are not normal constituents of human milk should be considered undesirable contaminants. In the present review, the following substances detected in human milk are considered: persistent organochlorine pesticides; polychlorinated biphenyls (PCB); polychlorinated dibenzodioxins (PCDD) and dibenzofurans (PCDF); polybrominated compounds; polycyclic aromatic hydrocarbons (PAH); trace elements; mycotoxins; nitrate, nitrite, nitrosamines; nicotine, caffeine, ethanol; and drugs. The levels of most of these substances found in human milk were within a range that would not constitute health hazards for breast-fed infants. For many ofthese, there is a comfortable safety margin. This applies also to organochlorine pesticides and PCB, particularly since, as a result of their discontinued use, the levels of these compounds have clearly declined in recent years. On the other hand, the aflatoxin burden mediated through breast milk, at least in certain tropical countries, appears to pose a definite health hazard. Detailed reference are given on the contamination of human milk with PCDD/PCDF which has to be considered as a matter of concern from the viewpoint of preventive public health. Although the low PCDD/PCDF levels found in the adipose tissue of infants indicate that there is no appreciable health risk emanating from these substances for breast-fed infants, appropriate measures to reduce the current rate of their emission into the environment have to be taken.

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“…In addition to exposure to airborne substances, the respiratory system is also exposed to chemicals via the systemic circulation [Lee et al 2000]. This is particularly true during gestation when the developing lungs are exposed to chemicals transferred from the maternal circulation, and during lactation when compounds are conveyed to the newborn via the mother's milk [Luck and Nau, 1984a]. Nicotine freely crosses the placenta [Lambers and Clarke, 1996] and is found in significant quantities in the milk of smoking mothers [Luck and Nau, 1984a].…”

Section: Metabolic Developmentmentioning

confidence: 99%

“…This is particularly true during gestation when the developing lungs are exposed to chemicals transferred from the maternal circulation, and during lactation when compounds are conveyed to the newborn via the mother's milk [Luck and Nau, 1984a]. Nicotine freely crosses the placenta [Lambers and Clarke, 1996] and is found in significant quantities in the milk of smoking mothers [Luck and Nau, 1984a]. Nicotine can therefore interact with the developing fetus and neonate in smoking mothers or mothers that are using NRT to quit smoking.…”

Section: Metabolic Developmentmentioning

confidence: 99%

Are nicotine replacement therapy, varenicline or bupropion options for pregnant mothers to quit smoking? Effects on the respiratory system of the offspring

Maritz

2009

Ther Adv Respir Dis

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Nicotine occurs 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 AMP 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 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. Since varenicline, a partial nicotine agonist, has basically the same structure as nicotine, and also binds to acetylcholine receptors in competition with nicotine (but with largely the same effect), it is not advisable to use nicotine or varenicline during gestation and lactation. Furthermore, the use of individual vitamin supplements is also not advisable because of the negative impact on the program that controls maintenance of lung structural and functional integrity and aging. A more appropriate smoking cessation program will also include a mixture of antioxidant nutrients such as in tomato juice.

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Nicotine and cotinine concentrations in serum and milk of nursing smokers.

Cited by 147 publications

References 26 publications

PPARγ agonist rosiglitazone prevents perinatal nicotine exposure-induced asthma in rat offspring

PPARγ agonist rosiglitazone prevents perinatal nicotine exposure-induced asthma in rat offspring

Nurturing and Breast-Feeding: Exposure to Chemicals in Breast Milk

Are nicotine replacement therapy, varenicline or bupropion options for pregnant mothers to quit smoking? Effects on the respiratory system of the offspring

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