Prenatal smoke exposure: Effects on infant auditory system and placental gene expression

Katbamna, Bharti; Klutz, Nicole; Pudrith, Charles; Lavery, J. Patrick; Ide, Charles F.

doi:10.1016/j.ntt.2013.04.008

Cited by 10 publications

(11 citation statements)

References 63 publications

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“…Prenatal exposure to nicotine seems to have adverse effects on hearing, which are detectable as early as in the neonatal phase as determined by otoacoustic emissions testing [9,10,11]. TSE is a chronic exposure, probably during a whole child’s life.…”

Section: Resultsmentioning

confidence: 99%

“…Some studies have suggested that maternal smoking during pregnancy can lead to intellectual delays, most likely caused by central nervous system impairment [25], or can negatively affect language ability through underlying physiologic mechanisms (e.g., the outer hair cells in the ear), thus leading to poorer performance on auditory processing tasks [26], temporal auditory processing [27], auditory brainstem responses [11,12,13] and attention deficit hyperactivity disorder [28]. The effects of maternal smoking during pregnancy on infants’ speech processing ability were previously investigated by event-related potentials (ERPs).…”

Section: Resultsmentioning

confidence: 99%

“…This new approach to study the cochlea improves the ways to investigate and interpret hearing loss. Recent findings suggest that the auditory functions in infants of smoking mothers were significantly reduced as measured by OAE [9,10] and auditory brainstem response [11,12,13]. …”

Section: Introductionmentioning

confidence: 99%

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Tobacco Smoke Exposure during Childhood: Effect on Cochlear Physiology

Durante

Pucci

Gudayol

et al. 2013

IJERPH

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The rate of smoking in Brazil is about 18.8%. Exposure to environmental tobacco smoke is one of the major factors predisposing children to several hazardous health problems. The objective of the present research was to analyze the effect of tobacco smoke exposure during childhood on cochlear physiology by measuring the transient evoked otoacoustic emissions (TEOAE) response levels. Cotinine, the main metabolite of nicotine, was measured in 145 students’ (8–10 years old) urine. Sixty students indicated tobacco smoke exposure (TSE) (cotinine urine levels ≥ 5.0 ng/mL) and 85 did not. The evaluation of TEOAE of TSE students showed lower response levels, mainly on frequencies of 2.8 kHz on the right and left ears and 2.0 kHz on left ear and lower signal noise response levels, mainly on the 1.0 kHz and 1.4 kHz frequencies, when compared to controls that were not exposed to tobacco. The mean hearing loss in tobacco smoke exposure children was 2.1 dB SPL. These results have important implications on the damage to the cochlear structures and indicate a possible loss in hearing and hearing ability development.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

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Tobacco Smoke Exposure during Childhood: Effect on Cochlear Physiology

Durante

Pucci

Gudayol

et al. 2013

IJERPH

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“…While the immediate ramifications are apparent, researchers have shown that nicotine exposure not only predisposes the fetus to lung dysfunction, but also has the ability to influence asthma in second and third generation offspring, likely through epigenetic modulation of the fetal program [140,141,142]. Aside from respiratory disorders, nicotine has further been shown to affect endocrine function [143,144], increase the likelihood of the fetus to develop chronic kidney disease (CKD) through increased mitochondrial dysfunction [145], and decrease auditory response and auditory development [146,147,148]. Overwhelming, the data suggests a particularly insidious role for SHS and its ability to influence development.…”

Section: Health Outcomes and Comorbiditiesmentioning

confidence: 99%

Plausible Roles for RAGE in Conditions Exacerbated by Direct and Indirect (Secondhand) Smoke Exposure

Lewis

Hirschi

Arroyo

et al. 2017

IJMS

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Approximately 1 billion people smoke worldwide, and the burden placed on society by primary and secondhand smokers is expected to increase. Smoking is the leading risk factor for myriad health complications stemming from diverse pathogenic programs. First-and second-hand cigarette smoke contains thousands of constituents, including several carcinogens and cytotoxic chemicals that orchestrate chronic inflammatory responses and destructive remodeling events. In the current review, we outline details related to compromised pulmonary and systemic conditions related to smoke exposure. Specifically, data are discussed relative to impaired lung physiology, cancer mechanisms, maternal-fetal complications, cardiometabolic, and joint disorders in the context of smoke exposure exacerbations. As a general unifying mechanism, the receptor for advanced glycation end-products (RAGE) and its signaling axis is increasingly considered central to smoke-related pathogenesis. RAGE is a multi-ligand cell surface receptor whose expression increases following cigarette smoke exposure. RAGE signaling participates in the underpinning of inflammatory mechanisms mediated by requisite cytokines, chemokines, and remodeling enzymes. Understanding the biological contributions of RAGE during cigarette smoke-induced inflammation may provide critically important insight into the pathology of lung disease and systemic complications that combine during the demise of those exposed.

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“…Kable and colleagues [34] found that the PTE level was negatively related to wave V latency and waves I–V interpeak latency intervals in 6-month-old infants. Katbamna et al [35] compared full-term, otherwise healthy infants from a group of mothers who smoked to a control group born to nonsmoking mothers using ABRs and distortion-product otoacoustic emissions (DPOAEs). DPOAE amplitudes were reduced in the infants with PTE.…”

Section: Introductionmentioning

confidence: 99%

Prenatal Exposure to Tobacco and Alcohol Alters Development of the Neonatal Auditory System

et al. 2021

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Prenatal exposures to alcohol (PAE) and tobacco (PTE) are known to produce adverse neonatal and childhood outcomes including damage to the developing auditory system. Knowledge of the timing, extent, and combinations of these exposures on effects on the developing system is limited. As part of the physiological measurements from the Safe Passage Study, Auditory Brainstem Responses (ABRs) and Transient Otoacoustic Emissions (TEOAEs) were acquired on infants at birth and one-month of age. Research sites were in South Africa and the Northern Plains of the U.S. Prenatal information on alcohol and tobacco exposure was gathered prospectively on mother/infant dyads. Cluster analysis was used to characterize three levels of PAE and three levels of PTE. Repeated-measures ANOVAs were conducted for newborn and one-month-old infants for ABR peak latencies and amplitudes and TEOAE levels and signal-to-noise ratios. Analyses controlled for hours of life at test, gestational age at birth, sex, site, and other exposure. Significant main effects of PTE included reduced newborn ABR latencies from both ears. PTE also resulted in a significant reduction of ABR peak amplitudes elicited in infants at 1-month of age. PAE led to a reduction of TEOAE amplitude for 1-month-old infants but only in the left ear. Results indicate that PAE and PTE lead to early disruption of peripheral, brainstem, and cortical development and neuronal pathways of the auditory system, including the olivocochlear pathway.

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Prenatal smoke exposure: Effects on infant auditory system and placental gene expression

Cited by 10 publications

References 63 publications

Tobacco Smoke Exposure during Childhood: Effect on Cochlear Physiology

Tobacco Smoke Exposure during Childhood: Effect on Cochlear Physiology

Plausible Roles for RAGE in Conditions Exacerbated by Direct and Indirect (Secondhand) Smoke Exposure

Prenatal Exposure to Tobacco and Alcohol Alters Development of the Neonatal Auditory System

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