Prenatal smoke exposure linked to adolescent hearing loss

Smoking on Waking Increases Risk of Lung and Oral Cancers
Smoking on Waking Increases Risk of Lung and Oral Cancers

Prenatal smoke exposure was significantly associated with adolescent hearing loss in a recent study, suggesting that mothers who smoke during their pregnancies may very well be damaging their children's auditory abilities.

“These novel findings suggest that in utero exposure to tobacco smoke may be injurious to the auditory system,” Michael Weitzman, MD, from the New York University School of Medicine, and colleagues reported in the Journal of the American Medical Association.

Hearing loss affects as many as 19.5% of adolescents between the ages of 12 and 19, while maternal smoking is reported in about 12% of pregnancies. Prenatal smoke exposure has been linked to childhood obesity and learning disabilities, and other studies have found associations between adult smoke exposure and increased risk of hearing loss, prompting the researchers to study a potential connection between maternal smoking during pregnancy and subsequent hearing loss.

The study gathered information about 964 adolescents aged 12 to 15 years from the National Health and Nutrition Examination Survey in the years 2005-2006. The presence of prenatal smoke exposure was determined by asking parents whether their child's biological mother smoked during the pregnancy. 

The study also examined the presence of current smoke exposure in the subjects through self-reports and measurements of cotinine, the major metabolite of nicotine and a commonly used indicator of both active smoking and second-hand smoke (SHS) exposure.

Hearing tests over a range of frequencies from 0.5 kHz to 8 kHz were administered on both ears for all participants. Sensorineural hearing loss (SNHL) was defined as having a pure-tone hearing threshold of more than 15 dB.

155 adolescents, or 16.1% of the population, had mothers who reported smoking during pregnancy. Across all measured frequencies, those with prenatal smoke exposure had higher pure-tone hearing levels on average. These figures were considered statistically significant at 6 kHz for the average hearing levels of both ears, and at 2 kHz and 6 kHz for hearing level in subjects' worse ear.

These frequencies were different from those that subjects with current SHS exposure had trouble with (2, 3 and 4 kHz), suggesting that the two forms of exposure may have different damaging effects on hearing.

Higher rates of SNHL in those with prenatal smoke exposure were seen for all levels of severity. The greatest discrepancy was seen when testing for unilateral low frequency hearing loss, which was 2.6 times more likely to affect exposed participants than unexposed.

The researchers hypothesized that prenatal maternal smoking causes metabolic dysfunction, fetal malnourishment and direct damage to the inner ear, which would explain the ensuing association with adolescent SNHL. They also noted that even though many of the mothers said they stopped smoking during the first trimester, a significant association to SNHL was still observed, implying that “even brief smoke exposure” can have “far-reaching consequences.”

The study's findings are “worrisome for many reasons” as other research has revealed relationships between prenatal smoking and poorer performance on auditory-related tasks, lower language and reading scores, higher risk of ADHD, and an increased likelihood to drop out of school prematurely.

Possible methods proposed to combat prenatal smoke exposure included increased smoking cessation programs and counseling for pregnant women. The study also suggested more auditory screening for adolescents, so that accommodations such as preferential classroom seating or hearing aids might be utilized if necessary.

The study cited several limitations, such as the lack of more information about the participants' mothers and the inclination to underreport smoking history.

by Walker Harrison, an undergraduate student at Columbia University and editorial intern with Clinical Advisor.


References

  1. Weitzman M et al. JAMA. 2013;doi:10.1001/jamaoto.2013.3294.
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