Purchase this article with an account.
Richard A. Stone, Lorri B. Wilson, Gui-shuang Ying, Chengcheng Liu, Jonathan S. Criss, Joshua Orlow, Jon M. Lindstrom, Graham E. Quinn; Associations between Childhood Refraction and Parental Smoking. Invest. Ophthalmol. Vis. Sci. 2006;47(10):4277-4287. doi: https://doi.org/10.1167/iovs.05-1625.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
purpose. Motivated by pharmacologic findings linking nicotinic acetylcholine receptors to eye development in chicks, the authors studied whether the refractions of children who were passively exposed to cigarette smoke by their parents differed from those of nonexposed children.
methods. A cross-sectional study was conducted among 323 patients (mean ± SD age, 8.7 ± 4.4 years; range, 1–20) in a tertiary care pediatric ophthalmology clinic. Half (162/323) of the subjects had strabismus. The accompanying parent completed a detailed questionnaire on parental smoking history and on putative risk factors for myopia. The results were compared to the subjects’ cycloplegic refractions.
results. If one or both parents ever smoked, their children had a lower myopia prevalence (12.4% vs. 25.4%; P = 0.004) and more hyperopic mean refractions (1.83 ± 0.24 vs. 0.96 ± 0.27 diopters; P = 0.02) than those whose parents never smoked. Smoking by either parent during the mother’s pregnancy had a similar effect on the child’s refraction. The associations largely persisted, both in multivariate models that included adjustments for the child’s age, child’s body mass index, child’s nearwork activity, parental myopia, and parental education and also in analysis by subgroups stratified by strabismus status.
conclusions. Despite the complex constituents of cigarette smoke, neuropharmacology perspectives may prove useful in the development of new hypotheses to understand the mechanisms governing refractive development, not only in experimental animals but also in children. The associations of less prevalent myopia and a more hyperopic mean refraction with both prenatal and childhood exposures to tobacco smoke suggest that nongenetic, environmental exposures may have long-term influences on refraction and that further study of the role of nicotinic acetylcholine receptors in refractive development is warranted.
This PDF is available to Subscribers Only