THE EFFECTS OF SMOKING / NICOTINE ON NIGHT VISION

 

by

 

Xxxxx X Xxxx (Contact me if needing reference)

 

 

 

 

 

 

 

 

Open-Book Examination 01 for Course ASCI 604 Submitted to the

 

Extended Campus

 

in Partial Fulfillment of the Requirements of the Degree of

 

Master of Aeronautical Science

 

 

 

 

 

 

 

 

 

Embry-Riddle Aeronautical University

 

Extended Campus

 

Giebelstadt Resident Center January 2004

 

 

 

 


ABSTRACT

 

Writer:             Xxxxx X Xxxx (Contact me if needing reference)

 

Title:                The Effects of Smoking / Nicotine on Night Vision

 

Institution:        Embry-Riddle Aeronautical University

 

Degree:           Master of Aeronautical Science

 

Year:               2004

 

Surprisingly few studies exist directly relating the effects of smoking on vision or in particular, night vision.  This may be attributed to the fact that tobacco use has already been labeled a dangerous and unhealthy practice.  Smoking and nicotine have been extensively studied and many of its physiological effects are understood.  They same holds true for the human eye and the complete visual system.  Comparing the two entities reveals many consistent relationships - most of which occur at the chemical level but also on the physical and neural levels.  An interesting correlation was found in an otherwise unrelated study on the photoreceptors of a flagellate.  Nicotine was used as the growth inhibitor of a protein very similar to rhodopsin.  Evident in most studies and documentation is nicotine and smoking always have some level of adverse effect on the body and the complex visual system - even if in minuscule amounts.


Table of contents

 

Abstract

 

I.          INTRODUCTION

 

II.          DISCUSSION

 

III.         CONCLUSIONS

 

IV.        RECOMMENDATIONS

 

REFERENCES

 

Page

 

4

 

5

 

15

 

17

 

20

 

 

 

 


I.    INTROduction

 

As the landmark of 100 years of powered flight has just passed it is easy to remember the Wright brothers first left the earth in a powered aero-craft as 1903 drew to a close.  Since that day, humans and all their unique physiological traits have been along for the ride.  Well before flying, however, humans were exposed to and using products that render them even less suitable for flying then they already are.  One such product is tobacco.

Years before the physical repercussions of tobacco were understood, and years before humans began to fly, tobacco was already a part of society.  Lorillard, the oldest tobacco company in America, for example, was established and producing cigarettes as early as1760 (cigarettes.com) - 143 years before the winged departure at Kill Devil Hill.  Another popular form of tobacco - smokeless chew or snuff - was, in fact, the first product of today’s tobacco giant, RJ Reynolds.  As early as 1875, Reynolds was making chewing tobacco available to the public (cigarettes.com).  Today, some aviators - both civilian and military - still use tobacco and are addicted to nicotine whether it is via smoking or smokeless chew.

It is difficult, if not impossible, to argue the single most important sensor a pilots uses while flying is vision.  This critical sense is highly susceptible to nicotine and it’s effects on the body, and the overall condition of the body itself has an impact on vision.  Any negative input to the visual system becomes more pronounced in low-light environments such as twilight hours or night flights.

 

II.    Discussion

 

Although we now know the many dangers nicotine presents the body, people still use it.  According to the American Psychological Association, “many researchers commonly name cognitive enhancement as one of the reasons smokers continue to smoke” (Azar, 1999).  The same could be said about chewers or dippers.  Regardless of the reason, nicotine is delivered to the body by both cigarettes and smokeless tobacco.  Smoking, however, adds additional and unique characteristics worthy of investigation.  For simplicity, the effects of nicotine and smoking are analyzed simultaneously but discernment is made if significant.

“There are several factors that make investigation of…smoking on night vision difficult” and published studies still show contradictions.  “Night vision is, in itself, a complex physiological process [which] encompasses many parameters [such as] scotopic dark adaptation, mesopic vision, contrast sensitivity [and] peripheral retinal sensitivity” (Kaspari).  Regardless of the difficultly, the visual system and its components are affected in specific ways from nicotine and/or smoke inhalation.  While some are dependent, many remain independent of the environment, and therefore, day vision and night vision are addressed as a whole.  It is critical to remember the human eye is not the most suitable piece of equipment for night vision so a less-than-ideal operating environment (night) compounds any physiological effect caused by smoking or nicotine.

 

NICOTINE AND THE BLOOD

 

Vigorous flow of oxygen-rich blood is essential to proper eye performance.  Nicotine and smoking negatively affect not only the quantity of flow but also the quality of blood flow. 

Blood Quantity.  The smoke from cigarettes introduces free radicals into the blood stream which in turn cause not only cellular damage, but are also cited for decreased nutrient flow to the lens and retina. Furthermore, these radicals substantially reduce the level of carotenoid and vitamin C concentrations in the blood (Kaspari).  Carotenoids “are a main dietary source of vitamin A in humans [and are] associated with reduced risk of…eye degeneration” (Young, 2002).  Vitamins are discussed in more detail later.

Obviously, the reduction of nutrients will reduce the efficiency of the lens and retina.  The lens refracts one third of the light entering the eye and is responsible for changing the focus from near to far and vice versa.  This process, also called accommodation, becomes more difficult as the lens hardens with age, but also if being robbed of required nutrients.  The retina holds the rods and cones, which are responsible for the conversion of light to electronic signals that our brain recognizes as images (Cyberco, 1995).  If not operating at full potential, the amount and rate at which light is processed is reduced and may potentially affect the transfer of electronic signals in the same way.

Poor blood circulation in the eyes can also be attributed to the erosion of the protective later separating the retina from our blood vessels.  Normally, these retinal cells are protected by plasma antioxidant - a natural substance carried by the blood.  The smoke by-products (i.e., not normally associated with smokeless tobacco) reduce the normal levels of plasma antioxidant (Kaspari).

According to Samuel Zelman (1973), the flow of blood is also reduced “by (1) vasospasm induce by nicotine, (2) atherosclotic narrowing of vessels, and (3) thrombotic occlusions.”  Vasospasm is caused by an irritation of the muscle tissue around blood vessels.  The irritation makes the muscles constrict around the vessels, decreasing their size and reducing blood flow (Gruen, 2000).  The vasospasms have further been shown to “cause enlargement of the normal blind spot and reduced threshold of differential brightness” (Zelman, 1973).  As there is no color in dark environments, it is this ‘differential brightness’ coupled with movement that allows us to see at night.  If this threshold is increased, the required differences of brightness must be greater if the eye is to perceive shapes or objects.  This presents a challenge during night sorties because aviators simply cannot affect the environment’s contrast or the available light (aside from spot or landing lights) - both of which would help increase the ‘differential brightness’.

Blood Quality.  Tobacco has such “an adverse effect on vision [because] it contains vast quantities of toxic chemicals” (Blindness, 1999).  Not only is tobacco highly toxic, the body readily absorbs it and only small amounts are required to trigger negative responses.  According to Wood (1944, p.65), nicotine is so poisonous, only “an extremely small dose [is] sufficient to bring about its…toxic effects”.  After only one cigarette, arterial blood rich in nicotine “reaches the brain in seconds.  This is faster than after an intravenous injection.  Nicotine overcomes the blood-brain barrier with ease” (Buchkremer, 1998).  Also, the levels of toxin are so great that the aftershock of one cigarette “causes a definite contraction of the blood vessels in the retina of the eye” (Wood, 1944, p.65).

Smoking has been shown to produce the retinal toxin cyanide.  Continued presence of cyanide can lead to toxic amblyopia.  “Amblyopia is reduced or dimness of vision…not related to visible changes in eye health” (Kaspari).  Toxic levels of methyl or wood alcohol have been found in smoke, and although the amount of these a daily smoker inhales is small, they have a dangerous cumulative quality.  Over time, it is possible enough could be absorbed to contribute to partial blindness (Wood, 1944, p.65)

 

CARBON MONOXIDE AND HYPOXIA

 

      As mentioned in the introduction, smoking incurs additional and different hazards simply because smoke and carbon monoxide (CO) is inhaled into the lungs.  Despite the physiological effects nicotine has on the body and the cardio system, Garland, Wise and Hopkin (1999, p.322) claim the “most significant impact of smoking…lies in the concomitant introduction of carbon monoxide into the pilot’s bloodstream.”  This problem is compounded by the design of human blood.  The oxygen-carrying hemoglobin has a very strong attraction for any CO present - more than 200 times stronger than the attraction to oxygen (O2).  This attraction essentially allows the CO to crowd out the O2, as our blood is unable to carry oxygen and CO molecules at the same time.  As a result, the total oxygen carrying capacity is reduced and a “temporary state of induced anemia” is produced (Garland, Wise and Hopkin, 1999, p.322).  Anemia is a condition resulting from a decrease of red blood cells (RBC) below the body’s normal level.  Since RBC carries O2, the body will receive less O2 required to function properly.  Normally, anemia results from low RBC production, too many RBC being lost, or if the body can’t reproduce faster than they are destroyed.  The causes range from serious disease to low levels of vitamins or iron to genetics (Amgen, 2002).  Smoking, however, can put the body under the same conditions even with robust levels of RBC.

      The rapid onset and strength of smoke’s toxins are similar with anemia as with the other physical effects mentioned earlier.  The amount of carboxyhemoglobin (CO mixed with blood) induced by only one cigarette has shown “significant negative effect on visual sensitivity although this CO content” is far lower than the level necessary to cause general discomfort (Garland, Wise and Hopkin, 1999, p.322).

      Carbon monoxides effects.  Engstrom (2003) indicates tests have shown a person’s tolerance for altitude is reduced by 5000 to 6000 feet due to the carbon monoxide from tobacco.  According to McFarland, Roughton, Halperin and Niven (1944), the effects of CO2 combined with a decrease of blood flow can increase the perceived altitude by as much as 50%.  In other words, the physiological effects a non-smoking pilot experiences at 15000 ft are similar to those felt at only 1000 ft after smoking.

      Miller and Tredici (1992) further expand on the effect of hypoxia on night vision.  The primary effect is an increase in the rod and cone threshold.  The decreased capability of the cones is demonstrated by the loss of color at hypoxic altitudes, but the “scotopic night vision at altitude can be significantly reduced.  Scotopic vision has been reported to decrease by 5 at 3500 ft, 20% at 10000 ft, and 35% at 13000 ft” (p.24).  It is interesting to note the 35% reduction in night vision occurs 5000 feet below the altitude requiring supplemental oxygen.

      The increase to the rod and cone threshold is a very critical point.  First, “below the intensity of moonlight, the cones cease to function and the rods alone are responsible for what is pure scotopic vision [or true night vision]” (AOA, 1992).  Secondly, if the intensity of a light continues to decrease, it first disappears from the cones (except the wavelengths of red) and eventually from the rods (lower intensity).  Therefore, if a person is flying in a low-light scenario (at night) his or her eyes are relying heavily on the rods, and if dark enough, entirely.  Additionally, if the intensity of the available light continues to decrease, the rods are also rendered ineffective.  If this person is experiencing any level of cigarette-induced hypoxia, their sole receptor (if dark enough), the rod, requires a higher intensity of light to function.

 

EYESIGHT AND NUTRITION

 

The eyes function as part of the body, therefore, it is unarguable that proper nutrition, mineral and vitamin intake is required to properly function.  However, even if a solid, healthy diet is adhered to, smoking and nicotine can negate these efforts.  The topic of nutrition is immense, but there is an interesting correlation between vision and nicotine in the realm of vitamins.

Vitamin A.  This vitamin, also known as carotene or beta-carotene (the difference mainly lies with source of intake, leafy plants vice fruits and vegetables), can aid in the formation of visual purple for scotopic vision.  Visual purple is a label for rhodopsin - a light-sensitive pigment in the rods and is discussed later.  Vitamin A has also been shown to minimize oxidization and the activity of free radicals (New Life, 2003).  Mentioned earlier, these free radicals cause cellular destruction and hinder nutrient flow. 

Vitamin B.  This vitamin is critical in helping the muscles of the eye function properly and circulating nutrients to the lens.  The specific B vitamin, Riboflavin (B2) keeps the eyes at a normal sensitivity to light.  If the levels of vitamin B are too low, eyes can become over sensitive to light resulting in fatigued and irritable eyes.  Also cataract and glaucoma patients routinely have low concentrations of vitamin B in their optics (Schnitzer (2003).

Vitamin C.  Vitamin C and A have an indirect relationship with their function in the visual system.  Stated above, vitamin A helps inhibit the activity of free radicals.  These radicals primarily destroy cellular membranes but also decrease the levels of vitamin C.  Vitamin C is imperative for healthy, robust circulation in the eyes.  Healthy lenses will have high concentrations of vitamin C.  Therefore, vitamin C - to maintain appropriate quantities and continue to function - depends on regular amounts of vitamin A.  In her summary of vitamins and visual impacts, Schnitzer (2003) explains that nicotine from tobacco burns vitamin A, stress quickly decreases the body’s store of all types of vitamin B, and “smoking zaps vitamin C levels.”

Radicals and Antioxidants.  Atoms with unusual (odd) number of electrons are called free radicals and are created when oxygen and certain molecules interact.  Free radicals are highly reactive and once they develop, they can start a chain reaction.  If cellular material, such as DNA, or the very critical cell membrane, reacts with radicals, the damage may be enough to cause the cell to function poorly, or worst case, die.  In order to prevent this type of damage, the body uses antioxidants as a defense mechanism.

Antioxidants and free radicals can safely interact, and the antioxidants essentially block the chain reaction before excessive damage occurs. Although the body has natural enzymes that search and destroy radicals, vitamins are the principle antioxidants - in particular, vitamin A (beta-carotene), E and C.  These must be supplied by diet, as the body itself cannot produce them (Jenkins, 1996).  As a result, any outside factor (smoking or chewing) that reduces these antioxidants does so from an already limited amount that the body has no natural ability to supplement, and the environment becomes more conducive to the destructive radicals.

 

MACULAR DEGENERATION

 

      Although macular degeneration (MD) usually happens later in life (age-related macular degeneration or AMD), its effects on vision can begin well before old age and are significant.  Found in the center of the retina, the macula is a small region (about the size of a pin head) directly opposite the lens (MD Foundation, 2003).  This area is has a very dense concentration of cones, and although not the principle player in scotopic vision, cones are still used with enough light and always used with sufficient red light.  Since the macula resides in the center of the eye, the primary night player - the rods - are normally unaffected as is peripheral vision.

      According to Sternberg (1996), low concentrations of antioxidants in the blood and insufficient flow of blood to the retina appear to contribute to macular degeneration.  “Smoking ranks as a risk factor because it reduces concentrations of these antioxidants and impairs circulation [to the retina].”

 

VISUAL PURPLE AND EUGLENA GRACILIS

 

In order to operate better at night, the human eye - like anything experiencing change - must become acclimated.  The process when eyes adjust or acclimate to changes in light intensity (from high to low) is referred to as dark adaptation.  The process includes mechanisms both physical and at the neural and chemical level (AOA, 1992).

Rhodopsin.  Chemicals, which are extremely light sensitive called photopigments, are found in both the cones and rods.  The pigment in the rods is called rhodopsin - also known as visual purple.  Three types of pigments reside in the cones (most likely corresponding to red, blue and green) but differ slightly from rhodopsin.

When exposed to light, these pigments (both in the rod and cone) begin a chemical reaction that changes the energy of light to electronic impulses.  These impulses then generate an ‘image’ after passed through the optic nerve.  This initial reaction is light adaptation and due to the reaction, the pigments are essentially ‘expended’ and decompose.  “Regeneration of the photopigments occurs during dark adaptation” (AOA, 1992).

When regeneration is complete, the eye is as adapted to the dark as it can become and the retinal sensitivity is at its highest.  The difference between rods and cones and their capability at night is where the difference lies.  The cones adapt much quicker (5-7 minutes) while the rods are complete in about 30-45 minutes.  The time is the duration to maximum sensitivity after exposed to bright light (AOA 1992).  At first, this seems counterintuitive, as the rods are more effective for scotopic vision.  However, cones operate best in well-lit environments so a quicker regeneration time is required to be effective.  Regardless of speed, “the cones…do not achieve the same level of sensitivity as the rods.  The rods slowly adapt to dim illumination, but eventually achieve a much greater sensitivity then the cones (AOA, 1992)”.

Euglena gracilis.  A rather obtuse but significant relationship exists between the flagellate Euglena gracilis and visual purple.  Barsanti, Passarelli, Walne and Paolo (2000) conducted experiments using Euglena to isolate and purify the protein that creates its photoreceptor.  Similar to the eye on a chemical level, Euglena - a flagellate that lives in small natural ponds - converts sunlight into energy and uses it for information.  The light spectrum absorbed by a single photoreceptor was measured.  As a result, “great similarity [existed] between these spectra and the absorption curve of rhodopsin.  [Therefore, the group] suggested a pigment such as a rhodopsin-like protein as the photoreceptive protein in Euglena.”  Eight years earlier, Barsanti and coworkers were able to inhibit formation of this photoreceptor through the use of nicotine (Barsanti et al., 2000).

With such similar chemical composition and physical response, it is fair to assume nicotine, whether absorbed through smoke or chew, would cause the human eye to suffer the same inhibition in the production of rhodopsin - thus inhibiting initial dark adaptation and re-adaptation if exposed to a higher intensity source of light.

 

iiI.   conclusions

 

      The negative effects of nicotine received via smokeless tobacco or cigarettes are no longer a mystery.  Tooth decay, emphysema, mouth cancer, respiratory problems and general poorer health are all attributed to tobacco.  Although the effects on vision are far from the focus of anti-tobacco campaigns and education, there are no less significant.  With an incredible reliance on vision, aviators must be aware how nicotine hinders both the physical eye and its capabilities.  Both smoking and chew serve as the conduit of nicotine to the bloodstream, and the nicotine gives the ‘high’ the user is seeking.  Smoking, however, presents additional health threats simply because the user is inhaling smoke.

      Smoking.  Smoking continues to become less and less accessible (and accepted) in social situations due to increasing numbers of smoke-free workplaces, smoking bans on almost every airline carrier and the threat of second-hand smoke.  However, there are pilots who continue to smoke.  The most significant impacts of smoking to vision appear to be from the smoke itself - outweighing those of the nicotine.  First of all, smoke is highly toxic and induces free radicals in the blood stream that have an abrasive effect - to the point of destruction - on cellular material.   Secondly, and according to Garland, Wise and Hopkin (1992, p.332), “the most significant impact of smoking” to the pilot is the addition of carbon monoxide to the bloodstream.  Carbon monoxide itself is a poison, but the greatest hindrance on vision stems from the follow-on hypoxia.  This not only decreases acuity, but also causes the pilot to suffer hypoxic symptoms of higher altitudes before physically reaching those altitudes.

      Nicotine.  Aside from smoking, another means of nicotine intake is via smokeless chew.  This product is likely a higher threat to the aviation community for several reasons.  First, it is easier to conceal and doesn’t have the obtrusive smoke aftermath.  Second, nicotine is transferred very quickly through direct contact with the highly sensitive gums.  Lastly, chew seems to better give the sensation of alertness (actually higher blood pressure), which like caffeine has an attractive value.  The drug of tobacco, nicotine, is most dangerous on a chemical level.  It reduces the body’s level of supplemental (vitamins) and natural antioxidants which are critical in the absorption of free floating radicals in the blood.  This is more significant when the nicotine intake is from cigarettes.  The smoke byproducts add free radicals and the nicotine reduces the body’s radical-fighting abilities.

Next, nicotine has a rapid effect on veins and arteries which reduces blood flow throughout the body.  Robust circulation is essential to the eyes and their function, and the problem is compounded in a high G environment.  The eyes now have to compete not only against the nicotine-induced reduction of venous diameter but also against the increased G loading.  Decreased visual field of view and a transfer to black and white (or gray vision) usually precedes gray or black outs.  It would stand to reason this is likely to happen at an increased onset rate and with fewer Gs if operating with below normal circulation.

Finally, and very critical to night vision is the inhibitory effect nicotine has on the production of visual purple or rhodopsin.  Nicotine has been shown to cease the formation of photoreceptors extremely similar to the human eye’s rhodopsin (Barsanti et al., 2000).  Rhodopsin is imperative to night vision as it is the chemical pigment responsible for dark adaptation.  As light decreases, or if a bright light is seen after being adapted, the eye must readapt to be effective.  Anything that slows this process - nicotine in this case - reduces capability for a longer period of time.

 

iV.  recommendations

 

      Reality Check.  According to Azar (1999), “no one to date has [found] whether nicotine can enhance performance in a significant way on real-world tasks.”  To believe tobacco improves ability and/or enhances alertness is to ignore the overriding negative effects on the human body.  Almost immediately after even one cigarette, chemical changes are taking place in the bloodstream which have an overall degrading effect.  Also, several of these changes (including residual toxins) have cumulative qualities making additional nicotine or smoke intake more dangerous.

      Time Out, Vitamins In.  If unable to stop smoking or chewing, aviators can limit the impact of nicotine to their night vision by avoiding tobacco use prior to sorties and supplementing their diets with vitamins.  The amount of time nicotine remains active is not definite as it varies from person to person.  Rosekind et al. (1996) compared nicotine’s duration to caffeine stating “it usually [remains] active for 3-5 hours, although the effects can continue for up to 10 hours in sensitive individuals.”  Additionally, Buchkremer (1998) labeled the radioactive half-life of nicotine concentration an average of two hours - also varying with the individual’s amount and schedule of input.  Comparing these figures, a safe estimate would be six hours to essentially rid the body of nicotine activity (assuming 1/8 radioactivity is insufficient - three half lives).  No smoking /chewing six hours prior to a sortie won’t completely rid the body of nicotine and other toxins but should reduce the intensity of any effects.

      Also, as nicotine robs the body of antioxidants it cannot manufacture, regular use of a complete multivitamin should help maintain a normal level.  If smoking or chewing is sufficient, however, additional supplements of vitamins A, B (complete) and C would be warranted.

Reduce or Cease Input.  Nicotine always impacts the body - even if in minute amounts - on a chemical or neural scale.  Vision is processed primarily on a chemical basis - turning impulses of light into electronic signals.  Additionally, “scotopic vision is of poorer quality; it is limited by reduced resolution…and provides the ability to discriminate only between shades of black and white” (AOA, 1992).  Therefore, any outside factor, such as nicotine, that negatively effects vision will be amplified in dark environments.  The bottom line, therefore, is to cease nicotine use, as it is the only sure way to avoid these effects.

 


REFERENCES

Amgen Incorporated.  Anemia Lifeline.  http://www.anemia.com/  (2002).

AOA (American Optometric Association).  “The Eye and Night Vision” http://www.aoanet.org/eweb/DynamicPage.aspx?site=AOAstage&WebCode=NightVision  (Adapted from the USAF Special Report, AL-SR-1992-0002 - see Miller et al. below) (1992).

Azar, B. “Nicotine as a performance enhancer?  Research results are spotty”. APA Monitor Online.  http://www.apa.org/monitor/jan99/nico.html (1999, Jan.).

Barsanti, Laura, Passarelli, Vincezo, Walne, Patricia L., and Gualteiri, Paolo.  “The photoreceptor of Euglena gracilis”.  Federation of European Biochemical Societies - FEBS Letters. http://www.elsevier.nl/febs/120/21/33/index.htt (2000).

“Blindness: How to Prevent Tobacco Induced Blindness”. The Crime Prevention Group. http://medicolegal.tripod.com/preventblindness.htm (1999).

Buchkremer, Gerhard, M.D.  Tabak - Abhängigkeit of the Deutsche Haupstelle gegen die suchtgefahren Neigung Gefahren (German Principle Establishment Against Addiction Dangers).  As translated from a German document (1998).

Cigarettes.com.  http://www.cigarettes.com/  (2002).

Cyberco.  “How the Eye Works”.  Excimer Laser (PRK) Information Site.  http://www.pixi.com/~gedwards/eyes/eyeanat.html  (1995).

Engstrom, Paul.  “Smoking: Hazardous to Your Aviation Health”.  I Fly America Online.   http://www.iflyamerica.com/smoking.htm   (2003).

Garland, Daniel J., Wise, John A., and Hopkin, V. David (1999).  Handbook of Aviation Human Factors.  Mahwah, New Jersey: Lawrence Erlbaum Associates, Publishers.

Gruen, John Peter, M.D. “Vasospasm”.  NeuroSurgery InfoNet. http://uscneurosurgery.com/  (2000).

Jenkins, Mark A., M.D.  “Antioxidants and Free Radicals”.  SportsMed Web. http://www.rice.edu/~jenky/sports/antiox.html (1996, June).

Kaspari, Linda.  “No Smoking”.  Macular Degeneration Support. http://www.mdsupport.org/library/nosmoke.html

MD Foundation.  “What is the macula?”  MD Research Fund.  http://www.eyesight.org/FAQ/faq.html  (2003).

Miller, Robert E. II and Tredici, Thomas J.  “Night Vision in Military Aviation”. Ophthalmology Branch, Armstrong Laboratory, Brooks AFB, TX. http://wwwsam.brooks.af.mil/web/af/courses/amp/AMP_Online/amp_Eye_lectures/UNV7.doc

New Life, A.  “Facts About Vitamin A…and the role organic vitamin A has within the body”.  http://www.anewlife.co.uk/vitamin_a.html  (2003).

Rosekind, M. R., Gander, P. H., Gregory, K. B., Smith, R. M., Miller, D. L., Oyung, R. L., Webbon, L. L., Johnson, J. M.  “Managing Fatigue in Operational Settings 1: Physiological Considerations and Countermeasures”.  Human Factors Research and Technology.  http://human-factors.arc.nasa.gov/zteam/fcp/pubs/j.beh.med1.html (1996).

Sternberg, S.  “Smokers risk vision loss in twilight years”.  Science News. http://www.sciencenews.org/sn_arch/10_12_96/fob2.htm  (1996, Oct 12).

Schnitzer, Debora.  “Nutrition and Vision”.  Feux d’Opale. http://users.skynet.be/sky52523/en/workshop/vision/nutrition.htm  (2003).

Wood, Frank L., M.D. (1944).  What You Should Know About Tobacco.  Wichita KS: The Wichita Publishing Co.

Young, Andrew J. “Carotenoids”.  International Carotenoid Society. http://www.carotenoidsociety.org/  (2002).

Zelman, Samuel, M.D. Correlation of Smoking History With Hearing Loss. 223 Journal of American Medical Association (8) (19 Feb 1973).  Sited by The Crime Prevention Group. http://medicolegal.tripod.com/preventblindness.htm  (1999).