Influences of maternal cigarette smoking on infant arousability

https://doi.org/10.1016/j.earlhumdev.2004.04.005Get rights and content

Abstract

Since the reduction in the incidence of the prone sleeping position, maternal cigarette smoking has become the strongest modifiable risk factor for Sudden Infant Death Syndrome (SIDS). This risk is dose dependent. Various mechanisms have been postulated to explain the increased risk of SIDS associated with maternal smoking, among these, impairment of arousal from sleep. This paper reviews the effects of maternal smoking on infant arousability from sleep, cardiorespiratory controls and sleep architecture.

Infants exposed to maternal smoking have been shown to have both decreased spontaneous and evoked arousability from sleep. Such impairment of arousal has been demonstrated to be associated with changes in control of autonomic cardiac function. Sleep architecture appears not to be altered by smoking.

During arousal, heart rate, blood pressure and breathing movements increase, while gross body movements occur to avoid the stimulus. Any impairment in arousability from sleep could occur when infants are exposed to maternal cigarette smoking, and could possibly contribute to the final pathway to SIDS.

Introduction

Maternal smoking has been associated with an increased risk of Sudden Infant Death Syndrome (SIDS) since the mid-1960s [1]. Since then, over 40 studies have examined maternal smoking and its association with SIDS, with the majority showing a positive association with a risk ratio of between 0.7 and 4.85 [2], [3]. In addition, a number of studies have shown that the risk of SIDS increases with the number of cigarettes smoked during pregnancy [3], [4], [5], [6], [7]. Moreover, paternal smoking and passive smoke exposure during infancy have been associated with an increased risk of SIDS, with some data demonstrating that these relationships are also dose-dependent [3], [5], [8]. Some authors now consider that maternal smoking, both before or after birth, is the major modifiable risk factor for SIDS following public health campaigns to reduce the incidence of prone sleeping [9].

Maternal smoking may also be a confounding risk factor for SIDS due to its association with other major risk factors such as low birth-weight, prematurity and/or intra-uterine growth restriction [5], [10], [11], [12]. Studies have also found that infants are at a greater risk of SIDS when sharing the parents' bed only if the mother smokes [13], [14].

As yet no mechanism that explains the final pathway of SIDS has been identified; however, a number of studies have implicated impairment in arousability [15], [16], [17]. In support of this idea, a prospective study examining differences in sleep characteristics in infants who subsequently died from SIDS found fewer body movements [18] and fewer awakenings from sleep compared with controls, especially at the end of the night when most SIDS occur [19]. Additionally, post-mortem examinations of infants dying of SIDS have identified abnormalities in brain regions associated with arousal [20].

Arousal from sleep is an important survival response to a life-threatening event such as hypotension or prolonged apnoea [15]. By arousing from sleep, heart rate, blood pressure and ventilation are increased [21], and a behavioural response is evoked allowing movement away from a potentially harmful stimulus [22].

Studies by ourselves and others have examined the effects of maternal smoking on infant arousability from sleep, cardiorespiratory control and sleep architecture. These studies are reviewed here.

Section snippets

Spontaneous arousal

A number of studies have demonstrated that spontaneous arousal from sleep is altered by exposure to maternal smoking.

In a study of 20 healthy term infants, 10 of which had mothers who reported smoking 10 or more cigarettes per day throughout pregnancy, in quiet sleep (QS), the proportion of obstructive apnoeas followed by arousal was significantly higher in the control group (32%) compared to the smoking group (4.7%, p=0.001). This was despite the fact that there was no difference in the number

Evoked arousal

A number of researchers have studied the effects of maternal smoking on evoked arousal in infants.

In a study comparing ventilatory and awakening responses to hypoxia (17%, 15% and 13% inspired O2) and hypercapnia (4%, 6% and 8% inspired CO2) during QS between infants of smoking mothers (n=13) and non-smoking mothers (n=34), Lewis and Bosque [25] found that more infants failed to awaken in response to hypoxia in the smoking group (15%) compared to the control group (54%) (p=0.006). Infants in

Autonomic control

It has been suggested that maternal smoking may alter autonomic control.

The effects of maternal smoking on autonomic control during both AS and QS were assessed by spectral analysis of heart rate in 18 infants (6–16 weeks postnatal age) from smoking and 18 infants from non-smoking mothers [32]. Smoking mothers smoked more than 10 cigarettes per day. Although birth weights tended to be lower in the smoking group, this did not reach statistical significance. Compared with non-smokers, infants

Sleep architecture

Several studies have examined the effects of maternal smoking on infant sleep architecture. No difference in total sleep time or duration of AS or QS epochs was found between infants exposed to maternal smoking and those who were not [24], [26], [31], [32], [36].

Other physiological parameters

In a large study of 509 infants, prenatal smoking was correlated with an increase in frequency and length of obstructive apnoeas in infants [36]. Mothers were divided into non-smokers (400), those who smoked 1–9 cigarettes/day (37) and those that smoked 10 or more per day (72). Both the number and duration of apnoeas were positively related to the number of cigarettes smoked, as was birth weight of the infants.

Maternal smoking has also been demonstrated to alter respiratory drive and the

General implications for SIDS

There is no doubt that maternal smoking both before and after birth increases the risk of SIDS [39], however, the mechanism by which maternal smoking acts is yet to be identified. The effects of maternal smoking during pregnancy on cardiorespiratory development and function before and after birth are poorly understood. Nicotine, the major constituent of cigarette smoke, readily crosses the placenta and has been found in fetal cord serum in concentrations generally 15% higher than those in

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      Specifically, prenatal and perinatal nicotine exposure upregulates GABAergic, glycinergic and serotonergic neurotransmitter systems that mediate inhibition (Luo et al., 2007; Cerpa et al., 2015), and nAChRs on hypoglossal motor neurons become desensitized (Pilarski et al., 2012). The associated physiological effects observed in animals and described in humans included increased frequency of central apnea, decreased hypoxic and hypercapnic ventilatory responses, reduced arousal responses, and the inability to autoresuscitate (Horne et al., 2004; Kahn et al., 1994; Hafstrom et al., 2005). For a complete overview of the effect of prenatal exposure to nicotine on central respiratory networks please see Campos et al. (2009).

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    This paper was compiled on behalf of the Sudden Infant Death Global Strategy Task Force.

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