Summary: Even prior to pregnancy, a mother’s exposure to second hand smoke can have implications for the brain development of her offspring, including damage to areas of the brain associated with emotion, memory and learning.
Source: Duke University Medical Center.
Findings raise caution for women of childbearing age.
Exposure to second-hand tobacco smoke — even before conception — appears to have a lingering impact that can later impair the brain development of a fetus, researchers at Duke Health report.
Using rats in experiments carefully designed to mimic the second-hand smoke exposures that humans encounter, the researchers found that the chemical components of tobacco smoke affect fetal brain development throughout pregnancy.
The smoke exposure damages regions of the brain involved in learning, memory and emotional responses. Although the impact was most severe with exposures occurring in late gestation, adverse effects on the fetuses’ neuro-development occurred even when the mothers were only exposed prior to conception.
“This finding has important implications for public health, because it reinforces the need to avoid secondhand smoke exposure not only during pregnancy, but also in the period prior to conception, or generally for women of childbearing age,” said Theodore A. Slotkin, Ph.D., professor in Duke’s Department Pharmacology & Cancer Biology.
Slotkin and colleagues, publishing in the January issue of the journal Toxicological Sciences, simulated secondhand smoke exposure by capturing and extracting the chemical compounds of tobacco smoke and administering the solution through implanted pumps in the laboratory animals.
That process eliminated the stress of breathing smoke, which in itself can potentially impact fetal brain development — a factor that had confounded earlier studies on the effects of tobacco smoke.
Groups of female rats received the tobacco smoke extract during one of three periods: prior to mating, early gestation or late gestation. The researchers then studied the offspring starting in early adolescence and into adulthood, focusing on brain regions that are known to be adversely affected by nicotine and tobacco smoke.
The researchers found that exposure to tobacco smoke extract in all three of the study periods resulted in the offspring having impaired function of the cholinergic brain circuits that govern learning and memory, and of the serotonin circuits that affect mood and emotional behavior.
It is not known how the smoke exposure damages fetal brain development prior to pregnancy. The researchers said more study is needed, but potential causes include the lingering effects of some of the smoke components, which can remain in the body for several days after exposure. They also suggested that the chemicals might change the mother rat’s metabolism or hormonal status, or they could be causing an epigenetic alteration in the egg, which affects the activity of genes that control brain function.
“Our study clearly shows there is no stage in which tobacco smoke is innocuous to the developing fetus,” Slotkin said. “We warn women about smoking during pregnancy, and most people are aware that secondhand smoke exposure is also harmful to the fetus, but our study is the first to show that exposure prior to conception is potentially damaging, as well. The public health implications should be obvious.”
A prior study from the same team found a substantial portion of the tobacco smoke effect resulted from the nicotine in the smoke. That finding suggests that e-cigarettes could also represent a significant hazard for women of childbearing age.
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In addition to Slotkin, study authors include Ashley Stadler, Samantha Skavicus, Jennifer Card, Jonathan Ruff, Edward D. Levin, and Frederic J. Seidler.
Funding: The research received funding from the National Institutes of Health (ES022831) and the U.S. Environmental Protection Agency (83543701).
Source: Sarah Avery – Duke University Medical Center Image Source: NeuroscienceNews.com image is credited to Kelly Higgins for Duke Health. Original Research:Abstract for “Critical Periods of Developmental Neurotoxicity for Tobacco Smoke” by Theodore A. Slotkin, Ashley Stadler, Samantha Skavicus, Jennifer Card, Jonathan Ruff, Edward D. Levin, and Frederic J. Seidler in Toxicological Sciences. Published online September 14 2016 doi:10.1093/toxsci/kfw180
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[cbtabs][cbtab title=”MLA”]Duke University Medical Center “The Harmful Effects of Second Hand Smoke Even Before Pregnancy: Mouse Study.” NeuroscienceNews. NeuroscienceNews, 5 January 2017.
<http://neurosciencenews.com/pregnancy-second-hand-smoke-5870/>.[/cbtab][cbtab title=”APA”]Duke University Medical Center (2017, January 5). The Harmful Effects of Second Hand Smoke Even Before Pregnancy: Mouse Study. NeuroscienceNew. Retrieved January 5, 2017 from http://neurosciencenews.com/pregnancy-second-hand-smoke-5870/[/cbtab][cbtab title=”Chicago”]Duke University Medical Center “The Harmful Effects of Second Hand Smoke Even Before Pregnancy: Mouse Study.” http://neurosciencenews.com/pregnancy-second-hand-smoke-5870/ (accessed January 5, 2017).[/cbtab][/cbtabs]
Critical Periods of Developmental Neurotoxicity for Tobacco Smoke
Secondhand tobacco smoke exposure in pregnancy increases the risk of neurodevelopmental disorders. We evaluated in rats whether there is a critical period during which tobacco smoke extract (TSE) affects the development of acetylcholine and serotonin systems, prominent targets for adverse effects of nicotine and tobacco smoke. We simulated secondhand smoke exposure by administering TSE so as to produce nicotine concentrations one-tenth those in active smoking, with 3 distinct, 10-day windows: premating, early gestation or late gestation. We conducted longitudinal evaluations in multiple brain regions, starting in early adolescence (postnatal day 30) and continued to full adulthood (day 150). TSE exposure in any of the 3 windows impaired presynaptic cholinergic activity, exacerbated by a decrement in nicotinic cholinergic receptor concentrations. Although the adverse effects were seen for all 3 treatment windows, there was a distinct progression, with lowest sensitivity for premating exposure and higher sensitivity for gestational exposures. Serotonin receptors were also reduced by TSE exposure with the same profile: little effect with premating exposure, intermediate effect with early gestational exposure and large effect with late gestational exposure. As serotonergic circuits can offset the neurobehavioral impact of cholinergic deficits, these receptor changes were maladaptive. Thus, there is no single ‘critical period’ for effects of low-level tobacco smoke but there is differential sensitivity dependent upon the developmental stage at the time of exposure. Our findings reinforce the need to avoid secondhand smoke exposure not only during pregnancy, but also in the period prior to conception, or generally for women of childbearing age.
“Critical Periods of Developmental Neurotoxicity for Tobacco Smoke” by Theodore A. Slotkin, Ashley Stadler, Samantha Skavicus, Jennifer Card, Jonathan Ruff, Edward D. Levin, and Frederic J. Seidler in Toxicological Sciences. Published online September 14 2016 doi:10.1093/toxsci/kfw180
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