Smoking and lens optical density Billy R. Hammond, a Billy R. Wooten, b Jose  E. Na Ân Äez a and Adam J. Wenzel a a Vision Science Laboratory, College of Arts and Sciences, Arizona State University West, Phoenix, AZ, USA and b Department of Psychology, Brown University, Providence, RI, USA Summary Epidemiological evidence indicates that smoking increases the risk of age-related cataract. No information is currently available, however, on the effects of smoking on the lens prior to catar- act development. In this study, we relate smoking behavior to lens optical density (OD) in younger individuals without frank cataract. Fifty three never smokers and 41 current smokers were compared directly. Thirty one past smokers were tested to examine the relationship between years since smoking cessation and lens OD. Lens OD was measured psychophysi- cally by comparing scotopic thresholds obtained at 410 (measuring) and 550 nm (reference). Stimuli were presented in Maxwellian view. The smokers in the sample smoked an average of 17.3 + / À 11.3 cigarettes/day for 20.4 + / À 12 years. No significant differences (other than in fat intake) were found between the smokers and nonsmokers in iris color, dietary patterns, or age. Despite their overall similarity, lens OD was significantly (p = 0.005) higher in the smokers. Moreover, we found a significant dose±response relationship (p = 0.02) between smoking fre- quency and lens OD. There was also a weak relationship between smoking frequency and lens OD for past smokers (p = 0.06), but no relationship between lens OD and years since smoking cessation. Our data indicate that smoking is directly related to age-related increases in lens OD throughout life and that these increases persist even after smoking cessation. # 1999 The Col- lege of Optometrists. Published by Elsevier Science Ltd. All rights reserved Introduction All of the pathological features that characterize age- related cataract (ARC) are exaggerations of changes found in the aging lens of normal individuals. In fact, no deterioration has been identi®ed in the cataractous lens that is not also present in the aged lens (reviewed by Young, 1991). This suggests that ARC is an exten- sion of the natural opaci®cation of the lens with age. Thus, studying factors related to individual dierences in lens senescence before cataract may provide import- ant information regarding the early etiology of ARC. Studying factors related to individual dierences in lens optical density (OD) may also be important because of the negative eects of a dense lens on visual performance. A dense lens can aect visual perform- ance, particularly in dim light (e.g., driving at dusk; Kosnick et al., 1988), by decreasing the amount of light reaching the retina (Klein et al., 1996). Moreover, denser lenses increase the amount of light that is scat- tered toward the retina which may reduce contrast sen- sitivity (van den Berg, 1996). Since lens transparency results from the short-range order of cytoplasmic proteins (Delaye and Tardieu, 1983), lens `senescence' is often quanti®ed by measur- ing lens OD. Post-translational modi®cation in the ordering of lens proteins (e.g., by aggregation) causes reduced transparency (and increased OD). Biochemical studies (Duncan et al.,1989; Mota et al., 1992) have shown that lens OD measured in vivo correlates highly with both morphological (e.g., aggregation of high molecular weight proteins) and physiological (lens membrane permeability) changes in the lens. Thus, it is reasonable to infer that increases in lens OD might sig- nal changes in the underlying health of the lens. This interpretation is consistent with evidence showing that lens OD is highest in patients with ARC (Sample et al., 1988) and longitudinal data on diabetics showing that lens OD increases monotonically until a cataract Ophthal. Physiol. Opt. Vol. 19, No. 4, pp. 300±305, 1999 # 1999 The College of Optometrists. Published by Elsevier Science Ltd All rights reserved Printed in Great Britain 0275-5408/99 $20.00 + 0.00 PII: S0275-5408(98)00085-4 Correspondence and reprint requests to: Dr. B.R. Hammond. Received: 26 August 1998 Revised form: 21 December 1998 300