Sudden Infant Death Syndrome and Smoking in the United States and Sweden

MacDorman, Marian F.; Cnattingius, Sven; Hoffman, Howard J.; Kramer, Michael S.; Haglund, Bengt

doi:10.1093/oxfordjournals.aje.a009260

Cited by 125 publications

(63 citation statements)

References 20 publications

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“…Indeed, chronic exposure of nAChRs to nicotine either in utero through maternal smoking or in perinatal life leads to irreversible brain damage (47) and constitutes a major independent risk factor for sudden infant death syndrome (46,48).…”

Section: Discussionmentioning

confidence: 99%

Nicotine activates immature “silent” connections in the developing hippocampus

Maggi

Magueresse

Changeux

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

104

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In the hippocampus at birth, most glutamatergic synapses are immature and functionally ''silent'' either because the neurotransmitter is released in insufficient amount to activate low-affinity ␣-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptors or because the appropriate receptor system is missing or nonfunctional. Here we show that, in the newborn rat, a brief application of nicotine at immature Schaffer collateral-CA1 connections strongly enhances neurotransmitter release and converts presynaptically silent synapses into conductive ones. This effect is persistent and can be mimicked by endogenous acetylcholine released from cholinergic fibers. Thus, during a critical period of postnatal development, activation of nicotinic acetylcholine receptors contributes to the maturation of functional synaptic contacts and the wiring of adult hippocampal circuitry.excitatory postsynaptic currents ͉ cholinergic stimulation ͉ Schaffer collateral-CA1 synapses ͉ presynaptic effect ͉ increased probability of glutamate release

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Section: Discussionmentioning

confidence: 99%

Nicotine activates immature “silent” connections in the developing hippocampus

Maggi

Magueresse

Changeux

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

104

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“…[201][202][203][204] Smoke in the infant's environment after birth is a separate major risk factor in a few studies, 202,205 although separating this variable from maternal smoking before birth is problematic. Thirdhand smoke refers to residual contamination from tobacco smoke after the cigarette has been extinguished 206 ; there is no research to date on the signifi-cance of thirdhand smoke with regards to SIDS risk.…”

Section: Smoking During Pregnancy In the Pregnant Woman's Environmenmentioning

confidence: 99%

SIDS and Other Sleep-Related Infant Deaths: Expansion of Recommendations for a Safe Infant Sleeping Environment

Moon¹

2011

Pediatrics

219

115

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Despite a major decrease in the incidence of sudden infant death syndrome (SIDS) since the American Academy of Pediatrics (AAP) released its recommendation in 1992 that infants be placed for sleep in a nonprone position, this decline has plateaued in recent years. Concurrently, other causes of sudden unexpected infant death occurring during sleep (sleep-related deaths), including suffocation, asphyxia, and entrapment, and ill-defined or unspecified causes of death have increased in incidence, particularly since the AAP published its last statement on SIDS in 2005. It has become increasingly important to address these other causes of sleep-related infant death. Many of the modifiable and nonmodifiable risk factors for SIDS and suffocation are strikingly similar. The AAP, therefore, is expanding its recommendations from being only SIDS-focused to focusing on a safe sleep environment that can reduce the risk of all sleep-related infant deaths including SIDS. The recommendations described in this report include supine positioning, use of a firm sleep surface, breastfeeding, room-sharing without bed-sharing, routine immunization, consideration of a pacifier, and avoidance of soft bedding, overheating, and exposure to tobacco smoke, alcohol, and illicit drugs. The rationale for these recommendations is discussed in detail in this technical report. The recommendations are published in the accompanying “Policy Statement—Sudden Infant Death Syndrome and Other Sleep-Related Infant Deaths: Expansion of Recommendations for a Safe Infant Sleeping Environment,” which is included in this issue (www.pediatrics.org/cgi/doi/10.1542/peds.2011-2220).

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“…It is now the most important independent risk factor contributing to the sudden infant death syndrome (SIDS) (1,2). The most compelling hypothesis for the link between smoking and SIDS is that nicotine in tobacco diminishes, among other things, crucial breathing and arousal responses to stress during sleep (3).…”

mentioning

confidence: 99%

β2 nicotinic acetylcholine receptor subunit modulates protective responses to stress: A receptor basis for sleep-disordered breathing after nicotine exposure

Cohen

Han²,

Grailhe³

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

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Nicotine exposure diminishes the protective breathing and arousal responses to stress (hypoxia). By exacerbating sleep-disordered breathing, this disturbance could underpin the well established association between smoking and the increased risk of sudden infant death syndrome. We show here that the protective responses to stress during sleep are partially regulated by particular nicotinic acetylcholine receptors (nAChRs). We compared responses of sleeping wild-type and mutant mice lacking the ␤2 subunit of the nAChR to episodic hypoxia. Arousal from sleep was diminished, and breathing drives accentuated in mutant mice indicating that these protective responses are partially regulated by ␤2-containing nAChRs. Brief exposure to nicotine significantly reduced breathing drives in sleeping wild-type mice, but had no effect in mutants. We propose that nicotine impairs breathing (and possibly arousal) responses to stress by disrupting functions normally regulated by ␤2-containing, high-affinity nAChRs.

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Sudden Infant Death Syndrome and Smoking in the United States and Sweden

Cited by 125 publications

References 20 publications

Nicotine activates immature “silent” connections in the developing hippocampus

Nicotine activates immature “silent” connections in the developing hippocampus

SIDS and Other Sleep-Related Infant Deaths: Expansion of Recommendations for a Safe Infant Sleeping Environment

β2 nicotinic acetylcholine receptor subunit modulates protective responses to stress: A receptor basis for sleep-disordered breathing after nicotine exposure

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