It’s no news that cigarette smoking has deleterious effects on health. It causes a broad spectrum of harm, including stained teeth, gum disease, wrinkles in the face/sagging skin and oral cancer.^1-3 It increases the risk of osteoporosis, lung cancer and cardiovascular disease. Smokers have reduced athletic ability, reproductive problems and early menopause, not to mention assorted ocular complications.¹

Large, population-based studies (the Rotterdam, the Physician’s Health and Nurse’s Health, Beaver Dam, Blue Mountain) have highlighted the perils of smoking and its effects on the eye, starting with the ocular surface and extending to the optic nerve. In addition to an increased risk of cataracts and retinal disease, the jury is still out regarding glaucoma and diabetic retinopathy, but several investigations have also shown an increased risk of these as well.¹

Thyroid function in smokers is adversely affected. Smokers show decreased levels of TSH and thyroglobulin, have obvious hypoxic effects on muscular tissue, and an overall decreased thyroid function.³ In addition, smokers appear to have a delayed response to treatment. Their thyroid-related eye disease is almost always exacerbated while smoking.

All forms of AMD carry a higher risk in smokers and former smokers. Studies have theorized that the risks are likely due to lipid peroxidation, decreased plasma antioxidants, retinal hypoxia/ischemia and induced ocular inflammation. Ischemic changes in smokers induced by vasoconstriction, increased blood viscosity, promotion of arteriosclerotic changes and decreased oxygen capacity in hemoglobin also contribute to ischemic optic neuropathy and retinal vascular occlusions.^1,2

Epidemiologic studies have clearly shown the attendant risks in smoking for contact lens wearers.^4-6 They have reduced corneal sensation, decreased tear film stability and an increased corneal punctate staining along with a tendency for increased lacrimal obstruction and decreased lysozyme concentration.^1,3 Lens wearers who smoke have a 4x greater risk of developing corneal infiltrates and a 3x greater risk of microbial keratitis.^4-6

The Lipopolysaccharide Link
Why is chronic smoking/exposure to smoke a risk to lens wearers? Might smoking simply be a surrogate for risky behavior or a link to bad hygiene? More likely, is there a direct, deleterious impact from the toxins rather than a grouping of confounders? The lipopolysaccharide (LPS) connection might just be the answer.

Lipopolysaccharides are the constituents of gram-negative bacteria outer membranes (endotoxins) and also contaminants of tobacco smoke. It can be recovered from the hands of any smoker, because tobacco smoke is contaminated with LPS.^7,8 This serves as a direct vector to the lens, and ultimately ends up in wearers’ eyes.

Pulmonologists are intrigued by LPS, which is responsible for the induction of proliferative airway changes in smokers.⁷ Chronic exposure to smoke and its toxins through LPS activates the toll-like receptors’ signaling pathway. This results in transcription of pro-inflammatory cytokines and initiation of innate immune responses. In smokers, LPS may be involved in bacterial infection-induced exacerbation in COPD patients. Perhaps this might explain the increased risk of inflammatory, and even infectious, responses in lens wearers who smoke.

As eye care practitioners, we are strategically poised to encourage patients to quit or reduce cigarette smoking, and also to care for those who continue to smoke. Counselors recommend the five “A”s: (1) ask each patient on every annual visit about their tobacco use; (2) administer clear, non-judgmental and personalized suggestions; (3) assess each patient’s readiness and interest in quitting; (4) assist and refer to appropriate counselors; and (5) arrange for adequate follow-up.⁹

Stayed tuned for additional information on any LPS connection as eye researchers look closely at the association in signaling pathways/inflammatory cascade thru Toll-like receptors in the cornea. In the meantime, we can have a significant impact with our patients on another front by encouraging smoking cessation.

1. Schornack M. Smoking and ocular conditions. Optom Times. 2013;2(2):27.
2. Available at: www.medicinenet.com/smoking_effects_pictures_slideshow/article.htm.
3. Thomas I, Jacob G, Abraham L, et al. The effect of smoking on the ocular surface and the precorneal tear film. Australian Med J 2012;5(4):221-6.
4. Szczotka-Flynn L, Lass J, Sethi A, et al. Risk factors for corneal infiltrative events in continuous wear of silicone hydrogel contact lenses. Invest Opththal & Vis Sci. 2010;51(11):5421-30.
5. Stapleton F, Keay L, Edwards K, et al. The incidence of contact lens related microbial keratitis in Australia. Ophthalmology. 2008; 115(10):1655-62.
6. Stapleton F, Edward K, Keay L, et al. Risk factor for moderate and severe microbial keratitis in daily wear contact lens users. Ophthalmology. 2012;119(8):1516-21.
7. Hasaday JD, Bascom R, Costa JJ, et al. Bacterial endotoxin is an active component of cigarette smoke. Chest. 1998;115:829-35.
8. Personal communication with Stan Huth, Abbott Medical Optics.
9. Available at: www.ucanquit2.org/helpsomeonequit/healthprofessionals/FiveAs.aspx