Chapter 210 – Epidemiology of Glaucoma

Chapter 210 – Epidemiology of Glaucoma






Epidemiology can be defined as “the study of the distribution and determinants of health-related states or events in specified populations, and the application of this study to control of health problems.”[1] In this chapter the distribution of glaucoma in the population (i.e., the prevalence and incidence) and its determinants (i.e., its risk factors) are discussed.

Most of the major epidemiological studies of glaucoma have been carried out in North America and Europe, areas in which primary open-angle glaucoma (POAG) is the most common form. Thus, most of the available data—especially population-based data—concern POAG; when data presented herein are not for POAG, this is stated explicitly.


The prevalence of a disease is “The number of instances of a given disease or other condition in a given population at a designated time.” [1] Citing an overall prevalence figure for glaucoma is almost meaningless because race, age, and possibly gender have such a profound effect that prevalence rates are best stated in relation to these variables.

Tables 210-1 and 210-2 summarize the results of the major population studies of glaucoma. Table 210-1 gives the results for Caucasian subjects, and Table 210-2 summarizes the studies that have involved African-American and African-Caribbean subjects.

The prevalence estimates vary in the studies, not only because of the different populations studied but also because of the different





Beaver Dam[3]



Blue Mountain[6]

Barbados Caucasians [7]

Baltimore Caucasians [2]

Age range studied (years)

Over 50


Over 55


Over 49


Over 40

Prevalence of primary open-angle glaucoma found (%)








Prevalence of ocular hypertension (%)














St Lucia[9]

Baltimore African-Americans [2]

Barbados African-Caribbeans [7]

London African-Caribbeans [10]

Age range studied (years)

Over 30

Over 40


Over 35

Prevalence of primary open-angle glaucoma found (%)







methods used to sample the populations and different definitions of glaucoma. However, the figures are reasonably consistent, with a prevalence of POAG in Caucasians over 40 years of age of around 2% and in African-Americans and African-Caribbeans over 40 years of age of around four times this.

Age has a major effect on glaucoma prevalence—for those of older age a higher prevalence of glaucoma exists. The Baltimore Eye Survey[2] found a prevalence of 1.23% in African-Americans of age 40–49 years but of 11.26% in those over 80 years of age; in Caucasians these values were 0.92% and 2.16%, respectively. The Beaver Dam study[3] found a prevalence of 0.9% in Caucasians of age 43–54 years and of 4.7% in those over 75 years of age. Similarly, the Roscommon[4] study found a prevalence of 0.72% in the age band 50–59 years but of 3.05% in those over 80 years of age. The studies shown in Tables 210-1 and 210-2 that had an upper age limit found lower prevalence rates for glaucoma (e.g., Dalby [5] ), which is consistent with the increasing prevalence with age.

The effect of gender on glaucoma prevalence is less certain. The Australian Blue Mountain Eye Study[6] found a slightly greater prevalence of POAG in women, the Barbados study[7] found an overall prevalence of POAG in men of 8.3% and in women of 5.7%, and the Rotterdam[8] study found a three times higher prevalence of POAG in men. However, other studies, which include the Baltimore,[2] Beaver Dam,[3] and Roscommon[4] studies, did not show a significant difference in prevalence between the sexes.

Few population studies have published figures for the prevalence of ocular hypertension. As Table 210-1 illustrates, the








Beaver Dam[3]


Blue Mountain[6]

Baltimore Caucasians [2]

Baltimore African-Americans [2]

Angle-closure glaucoma, narrow angles







Pseudoexfoliative glaucoma







Other secondary glaucomas









Roscommon[4] and Blue Mountain[6] studies had similar results of 3.6% and 3.7%. What the majority of population studies do show is that the prevalence of glaucoma associated with high intraocular pressure (IOP) is relatively rare. The Beaver Dam[3] study found that 25% of the subjects with definite POAG had IOPs <21?mmHg (<2.8?kPa).

For the reasons mentioned in the introduction, prevalence figures for non-POAGs are harder to come by. The findings of the major studies are summarized in Table 210-3 . Glaucoma associated with narrow drainage angles is uncommon—although to compare different studies is difficult because of variations in the diagnosis of angle closure. Table 210-3 indicates prevalences from 0.04% in the Beaver Dam[3] study to 0.9% in Baltimore African-Americans.[2] Quigley[11] has calculated the prevalence of angle-closure glaucoma from nine European studies to be about 0.2% for those over 40 years of age.

Angle-closure glaucoma is thought to be less common in those of African descent—Quigley[11] suggests that about half the European rate applies. However, Luntz[12] has found an equal prevalence in South African Caucasians and Africans. In Asian populations, angle-closure glaucoma is the type found most commonly. A Japanese study found a prevalence of angle-closure glaucoma of 0.31%,[13] and those of Chinese origin have higher rates of angle-closure glaucoma than any other group—three times more common than POAG.[11]

The true prevalence of pseudoexfoliative glaucoma is difficult to determine, as some studies did not classify it separately from POAG and for studies in which the subjects were not dilated, underdiagnosis is likely. It is commonly thought to be more prevalent in those of Scandinavian origin, but the Dalby[5] study from Sweden found a prevalence of only 0.07%, whereas the Roscommon [4] study (Republic of Ireland) had a 1.33% prevalence. High prevalences of pseudoexfoliative glaucoma have been noted in Africans from South Africa but not in African-Americans. [12]

Other secondary glaucomas are rarely studied as separate entities in population studies. The Roscommon[4] study found two cases out of 2186 subjects examined (one aphakic and one thrombotic); the Dalby[5] and Blue Mountain[6] studies found similar prevalences of 0.27% and 0.2%, respectively. Quigley[11] calculated a mean prevalence from eight studies (Europe, Africa, and Asia) of about 0.44%.


Incidence is defined as “The number of instances of illness commencing, or persons falling ill, during a given period in a specified population.” [1] Difficulties in the diagnosis of early glaucoma and the need to follow a cohort for many years make true incidence figures difficult to obtain for glaucoma. In the Bedford survey an average annual incidence of 0.048% was found,[14] and Armaly et al.[15] studied 3936 patients over 7 years and found that 4 developed POAG, to give an annual incidence rate of about 0.025%.

The incidence of glaucoma rises with age. Results from statistical modeling indicate that for a general population of Caucasians, the incidence rises from 0.08 per 1000 per year for those in their early 40s to 1.46 per 1000 per year to those in their



Main Risk Factors for Glaucoma











Intraocular pressure


Optic nerve head










Systemic hypertension




Family history




Cigarette smoking


Alcohol intake


Socioeconomic factors





80s.[16] It seems likely that these incidence figures are higher in African-American and African-Caribbean populations.


A risk factor is defined as “An aspect of personal behavior or lifestyle, an environmental exposure, or an inborn or inherited characteristic, which on the basis of epidemiological evidence is known to be associated with health-related conditions important to prevent.”[1] Large, population-based studies provide valuable insights into risk factors for the development of glaucoma, whereas hospital-based studies are subject to selection bias. Good examples of this selection bias occur with patients who have myopia and diabetes—conditions for which regular eye examinations are likely, as a result of which the opportunity for glaucoma to be diagnosed is increased. Thus, hospital-based studies tend to overestimate the proportion of glaucoma patients who also have myopia and diabetes and so implicate these diseases as risk factors for glaucoma.

Population-based studies are more useful than those that are hospital based, but this advantage is lost if the study subjects are not selected randomly. If, for example, the protocol of the study is to ask for volunteers, it is those who have greater concerns about glaucoma, for example, those who have a family history, who are more likely to present for examination. If the sample is not truly random, the influence on glaucoma of such factors as family history is overestimated. The main risk factors for glaucoma that have been examined in population studies are classified in Box 210-1 .

Demographic Risk Factors


The prevalence and incidence figures shown indicate that increasing age is a major risk factor for glaucoma. In fact, this trend has been found in all population-based studies of glaucoma in which age has been examined.[16] As well as being consistent across various studies, the magnitude of increase is uniformly large with prevalence rates 4–10 times higher in the oldest age group compared with the baseline (usually subjects in their 40s).[2] [3] [4] [7]


The Baltimore,[2] Beaver Dam,[3] and Roscommon[4] studies did not find either men or women to be at a significantly



greater risk of glaucoma. However, the Barbados[7] Eye Study did find that men have an age-adjusted risk of 1.4 compared with women, and the Rotterdam[8] study found a three times increased risk for men. Conversely, the Dalby[5] study indicated a higher risk for women.

Overall it seems unlikely that gender is a major risk factor for the development of glaucoma.


For some time, it has been suspected that individuals of African, African-American, and African-Caribbean origin are at higher risk of POAG, but it is only relatively recently that this has been confirmed by large-scale population studies.

The Baltimore Eye Survey[2] found a fourfold excess prevalence in African-Americans compared with Caucasians. The Beaver Dam[3] study found an overall prevalence of 2.1% in an all-Caucasian population, which compares with a prevalence of 8.8% in the St. Lucia study[9] in which all the participants were African-Caribbean. The African-Caribbean Eye Survey [10] showed a relative risk for glaucoma of 3.7 in Haringey (London) African-Caribbeans compared with Roscommon[4] Caucasians.

The Barbados[7] study found a gradient in prevalence by racial group, with the highest risk in those who described themselves as black; a lower prevalence was found in those who classified themselves as of mixed race, and the lowest prevalence was for those who were white. Interestingly, the London African Caribbean study[10] showed a statistically significant association between IOP and skin color (but not between skin color and glaucoma).

Not only does a higher prevalence of POAG exist among black racial groups, but there is good evidence that the onset of the disease occurs at a younger age in these groups.[17] A study in Malawi found a large number of glaucoma subjects in the age range 20–30 years. Similarly, the average age of glaucoma patients in Jamaica was found to be 10 years less than the average in America. Wilson et al. [18] found that the average age at presentation for patients of African origin was 49.5 years while for Caucasians it was 59.8 years.

Ocular Risk Factors


Although little doubt exists that raised IOP is a major risk factor for glaucoma, it is not as fundamental as it was once thought to be. There is strong evidence that IOP is associated intimately with glaucoma:

• The Baltimore study results indicate that the prevalence of POAG rises with increasing IOP.[19]

• The visual field loss of patients whose IOP is lowered by whatever means is usually slowed.[20]

• If an individual has glaucoma, the eye that has the higher IOP tends to lose field more quickly—this occurs even if both IOPs are <21?mmHg (2.8?kPa).[21]

• For studies in which IOP is excluded from the definition of glaucoma (as it should always be), it is related strongly to the risk of glaucoma,[10] as illustrated in Figure 210-1 (taken from the prevalence of POAG in the Baltimore Eye Survey[19] ).

It is important to note that the relative risk of glaucoma begins to rise (i.e., is greater than 1) from about 16?mmHg (1.7?kPa). The commonly used cutoff between “normal tension” glaucoma [=21?mmHg (=2.8?kPa)] and “high tension” glaucoma [>21?mmHg (>2.8?kPa)] is therefore questionable.

A similar point is illustrated in Figure 210-2 , taken from Davanger et al.,[22] who plotted IOP level against the probability of having glaucoma as calculated from their own population survey. Figure 210-2 shows that although a very high IOP [35?mmHg (4.7?kPa) or more], if sustained, sooner or later results in glaucomatous damage, it is not inevitable that IOPs below this level always result in glaucomatous damage. For example, those who have an IOP of 27?mmHg (3.6?kPa) have a 50% chance of glaucoma development, whereas those who have an IOP of 23?mmHg (3.1?kPa) have only a 10% chance.

The use of the terms normal tension and low tension glaucoma is not very helpful. A more realistic concept is to consider



Figure 210-1 The risk of primary open-angle glaucoma at various levels of intraocular pressure. (Adapted with permission from Sommer A, Tielsch JM, Katz J, et al. Relationship between intraocular pressure and primary open angle glaucoma among white and black Americans. Arch Ophthalmol. 1991;109:1090–5.)



Figure 210-2 The probability of primary open-angle glaucoma at various levels of intraocular pressure. (Adapted with permission from Davanger M, Ringvold A, Bilka S. The probability of having glaucoma at different IOP levels. Acta Ophthalmol. 1991;69:565–8.)

that an individual’s optic nerve has a level of IOP that it can or cannot withstand. At a clinical level this is manifest by the presence or absence of visual field decline. If field loss occurs, the IOP of the patient needs to be reduced to a level that stops (or more realistically slows) this decline.

That IOP is a major risk factor for glaucoma rather than a diagnostic requisite means that some other factor or factors act with higher pressures in the eye to produce the characteristic glaucomatous changes.


As well as being an important marker of the presence and advancement of glaucoma, the structure of the optic nerve head may play a role in the pathogenesis of glaucoma. Two main theories exist for the mechanism of optic nerve damage in glaucoma. [21] The mechanical (IOP-related) theory suggests that the pressure head acts directly on the lamina cribrosa. The lamina cribrosa is not supported well superiorly and inferiorly at the disc, and it is here that the initial damage occurs to produce the characteristic arcuate defects. Variations in ganglion cell support at the disc may explain the



variations between IOP susceptibilities of individuals with similar IOPs.

The alternative theory is the vascular mechanism of damage—in which changes within the microcirculation of the disc capillaries are responsible for glaucomatous changes. Whether this is primarily vascular or secondary to IOP has not been elucidated.

Epidemiological studies have implicated disc variation as a risk factor for glaucoma; both vertical and horizontal cup:disc ratios correlate positively with subsequent field loss. The Collaborative Glaucoma Study[13] indicated that a high ratio is a risk factor for the development of field defects.

One of the proposals to explain why African racial groups have a greater prevalence of POAG than Caucasians—despite no differences in the IOP patterns—is that African racial groups have been noted to have larger discs and larger cup:disc ratios than Caucasians. Larger discs and discs with large cup:disc ratios have been found to be more susceptible to glaucomatous damage.[21]


Myopia has been associated with an increased risk of POAG for a long time.[14] However, the majority of the studies that show this association are hospital based and subject to the hospital bias mentioned previously. If an increased risk of POAG exists in myopes, it is likely to be overestimated.


High degrees of hypermetropia are related strongly to angle-closure glaucoma—both the acute and chronic types.

Systemic Risk Factors


As with myopia, diabetes has long been implicated as a risk factor for POAG and, as with myopia again, the risk associated with it is based on hospital studies and is overestimated. Conversely, the large population studies either have not found diabetics to be at greater risk of POAG or have found a much smaller effect than that in the hospital-based studies.[7] [10] [23]


Studies of the role of blood pressure in the pathogenesis of glaucoma, like those of diabetes, are bedeviled by hospital bias. A number of studies have noted a direct relationship between rise in blood pressure and rise in IOP,[24] but it has been harder to find a similar association between blood pressure and POAG.

The Baltimore Eye Survey investigators recognized that simply to compare the blood pressure of individuals with and without glaucoma would be unlikely to provide a definitive answer and so examined the vascular perfusion pressure of their subjects.[24] The perfusion pressure is the blood pressure (systolic, diastolic, or mean) minus the IOP; the subjects in the study showed a strong association between the prevalence of POAG and low diastolic perfusion pressure, as illustrated in Figure 210-3 . The graph indicates that the subjects with diastolic perfusion pressures below 30?mmHg (4.0?kPa) have a six times higher age-adjusted risk of POAG than those with pressures of 50?mmHg (6.7?kPa) or greater.

The hypothesis is that optic nerve damage may occur in these subjects because of poor optic nerve perfusion. This theory is enhanced further by the results of 24-hour blood pressure monitoring, which show that patients with profound falls in their blood pressure overnight (“nocturnal dippers”) have an increased risk of POAG.

A further refinement of the hypothesis also comes from the Baltimore Eye Survey, which showed that younger subjects (less than 60 years of age) with raised blood pressures have a lower risk of POAG than the age-matched normal population. Conversely, older subjects (over 70 years of age) have a higher risk than their aged-matched controls. A reason for this may be that hypertension actually improves optic nerve head flow initially, but when secondary vascular changes have occurred (after prolonged hypertension), resistance to blood flow increases.

The two findings of the Baltimore Eye Survey may be related in that the vascular changes of prolonged hypertension result in loss of blood vessel autoregulation, which reduces the ability of the nerve head vessels to respond to a reduction in diastolic perfusion.



Figure 210-3 The relationship between the prevalence of primary open-angle glaucoma and diastolic perfusion pressure of subjects from the Baltimore Eye Survey. (Adapted with permission from Tielsch JM, Katz J, Sommer A, et al. Hypertension, perfusion pressure and primary open-angle glaucoma. Arch Ophthalmol. 1995; 113:216–21.)

It is important to stress that this theory, although elegant, still requires far more evidence.

Genetic Risk Factors

Little doubt exists that a positive family history of glaucoma places an individual at increased risk of glaucoma. Estimates of POAG cases being familial vary in the range 13–47%, and a 5–20 times prevalence rate occurs in those who have a positive family history. Specific families have been found that indicate an autosomal dominant pedigree, whereas others appear to have a recessive gene.

However, studies of family history and glaucoma are prone to bias—which probably explains the widely differing prevalence rates in different studies. A patient who knows that a member of the family has glaucoma is more likely to present to the clinic and is more likely to attend for surveys. Also, family history data are provided by the patient and can be subject to recall bias.

The most accurate estimate of the association of family history and risk of developing glaucoma is from unbiased population studies that have a high response rate, such as the Baltimore Eye Survey.[25] This showed that family history is a significant risk factor for POAG but to a lesser extent than in most other published studies. The odds ratio of having POAG for those with siblings who had the disease was found to be 3.69; for those with parents who had the disease the ratio was 2.17 and for those with children who had the disease, 1.12.

Other Proposed Risk Factors


Although much studied, smoking cigarettes usually has not been shown to be a risk factor for glaucoma. Katz and Sommer,[26] in a hospital-based, case-control study, found no association between smoking and glaucoma. Most convincingly, the Beaver Dam study, which is the largest of any of these studies, did not show a relationship between smoking and POAG.[27]


A number of studies have shown a link between alcohol consumption and the risk of glaucoma. Katz and Sommer[26] found an association between glaucoma and alcohol use, but only in Caucasian patients. However, once again it seems likely that studies that are not population based are biased, for heavy drinkers have more contact with health services and, therefore, increased opportunity to have the glaucoma diagnosed.







Hiller and Kahn [29]


Leibowitz et al. [31]

Ghafour et al. [32]

Aclimandos and Galloway [33]

Year published












Percentage of blind registered with glaucoma






This is given as a proportion of the total number of registered blind for each country and year of publication.



Thus, when alcohol intake is looked at on a population basis, as in the Beaver Dam study,[27] no suggestion exists of a relationship between alcohol and glaucoma.


Leske and Rosenthal[28] postulated that the factors that influence access to adequate medical care, such as income, educational level, and socioeconomic status, would have an effect on the occurrence of glaucoma. Relatively little work has been done on this aspect of glaucoma; one study found a higher prevalence of glaucoma in outdoor manual workers than in indoor workers (the latter having the higher income). A similar study found a higher rate of glaucoma in manual laborers compared with clerical workers—although this was not controlled for race.[28]


Glaucoma, in all its forms, is a major cause of irreversible blindness throughout the world. It was calculated that 6.7 million people would be blind from the disease by the year 2000.[11] A number of studies indicate that, in the developed nations, the health services are aware of only 50% of the total number of people who have glaucoma, and it seems highly likely that this percentage is much smaller in the developing countries. [4]

Blind registration statistics offer one method by which to estimate the burden of glaucoma blindness. Table 210-4 illustrates the results of some published studies of blind registration figures. Although the percentages are fairly consistent in different countries and over time, the data from which these are drawn are subject to certain biases. Blind registration data have a number of flaws and usually are regarded as an underestimate of the true blindness figures.

Population estimates of glaucoma blindness are less prone to bias. For the Roscommon study[4] cohort a prevalence of blindness of 7.3% was found; the Baltimore Eye Study [34] had a visual impairment figure of 4.4% overall but higher in African-American subjects (at 7.9%).

The latter finding is consistent with other studies that indicate a higher rate of blindness in patients of African origin. Whereas glaucoma is the third highest cause of blindness registration in the United States, it is the most common cause of blindness registration among African-Americans. Hiller and Kahn[29] found a rate of glaucoma blindness seven times higher for non-Caucasians than Caucasians. The difference persisted across all age groups and both sexes and was not due to differential registration, as the age-specific rates of registered blindness were also higher for non-Caucasians.


Little doubt exists that the glaucomas represent a major public health problem in all parts of the world. At the individual level, they represent a particularly severe form of blindness that, unlike cataract, is irreversible. Although the underlying pathogenesis of glaucoma is not understood fully, the therapeutic maneuver of reducing IOP seems to slow progression of the disease in the majority of sufferers. Early diagnosis thus appears to offer the best way to maximize the number of years of sight for the patient who has glaucoma.





1. Last JM. A dictionary of epidemiology, 2nd ed. Oxford: Oxford University Press; 1988.


2. Tielsch JM, Sommer A, Katz J, et al. Racial variations in the prevalence of primary open angle glaucoma. JAMA. 1991;266:369–74.


3. Klein BEK, Klein R, Sponsel WE, et al. Prevalence of glaucoma. Ophthalmology. 1992;99:1499–504.


4. Coffey M, Reidy A, Wormald R, et al. Prevalence of glaucoma in the west of Ireland. Br J Ophthalmol. 1993;77:17–21.


5. Bengtsson B. The prevalence of glaucoma. Br J Ophthalmol. 1981;65:46–9.


6. Mitchell P, Smith W, Attebo K, Healey PR. Prevalence of open-angle glaucoma in Australia. Ophthalmology. 1996;103:1661–9.


7. Leske MC, Connell AMS, Schachat AP, Hyman L. The Barbados Eye Study—prevalence of open angle glaucoma. Arch Ophthalmol. 1994;112:821–9.


8. Dielemans I, Vingerling JR, Wolfs RCW, et al. The prevalence of primary open-angle glaucoma in a population based study in the Netherlands. Ophthalmology. 1994;101:1851–5.


9. Mason RP, Omofosalade K, Wilson MR, et al. National survey of the prevalence and risk factors of glaucoma in St Lucia, West Indies. Ophthalmology. 1989;96:1363–8.


10. Wormald RPL, Basauri E, Wright LA, Evans JR. The African Caribbean eye survey: risk factors for glaucoma in a sample of African Caribbean people living in London. Eye. 1994;8:315–20.


11. Quigley HA. Number of people with glaucoma worldwide. Br J Ophthalmol. 1996;80:389–93.


12. Luntz MH. Primary angle-closure in urbanized South African Caucasoid and Negroid communities. Br J Ophthalmol. 1973;57:445–56.


13. Shiose Y, Kitazawa Y, Tsukahara S, et al. A collaborative glaucoma survey for 1988 in Japan. Rinsho Ganka. 1990;44:653–9.


14. Perkins ES. The Bedford glaucoma survey: 1. Long term follow-up of borderline cases. Br J Ophthalmol. 1973;57:179–85.


15. Armaly MF, Krueger DE, Maunder L, et al. Biostatistical analysis of the collaborative glaucoma study. 1. Summary of report of the risk factors for glaucomatous visual field defects. Arch Ophthalmol. 1980;98:2163–71.


16. Tielsch JM. The epidemiology of primary open angle glaucoma. Ophthalmol Clin North Am. 1991;4:649–57.


17. Clarke EE. A comparative analysis of the age distribution and types of primary glaucoma among populations of African and Caucasian origins. Ann Ophthalmol. 1973;5:1055–71.


18. Wilson R, Richardson TM, Hertzmark MA, Grant WM. Race as a risk factor for progressive glaucomatous damage. Ann Ophthalmol. 1985;17:653–9.


19. Sommer A, Tielsch JM, Katz J, et al. Relationship between intraocular pressure and primary open angle glaucoma among white and black Americans. Arch Ophthalmol. 1991;109:1090–5.


20. Jay JL, Murdoch JR. The rate of visual field loss in untreated primary open angle glaucoma. Br J Ophthalmol. 1993;77:176–8.


21. Sommer A. Glaucoma: facts and fancies. Eye. 1996;10:295–301.


22. Davanger M, Ringvold A, Bilka S. The probability of having glaucoma at different IOP levels. Acta Ophthalmol. 1991;69:565–8.


23. Dielemans I, De Jong PTVM, Stolk R, et al. Primary open angle glaucoma, intraocular pressure and diabetes mellitus in the general elderly population. Ophthalmology. 1996;103:1271–5.


24. Tielsch JM, Katz J, Sommer A, et al. Hypertension, perfusion pressure and primary open-angle glaucoma. Arch Ophthalmol. 1995;113:216–21.


25. Tielsch JM, Katz J, Sommer A, et al. Family history and risk of primary open angle glaucoma. Arch Ophthalmol. 1994;112:69–73.


26. Katz J, Sommer A. Risk factors for primary open angle glaucoma. Am J Prev Med. 1988;4:110–14.


27. Klein BE, Klein R, Ritter LL. Relationship of drinking alcohol and smoking to prevalence of open angle glaucoma. Ophthalmology. 1993;100:1609–13.


28. Leske MC, Rosenthal J. Epidemiological aspects of open angle glaucoma. Am J Epidemiol. 1979;109:250–72.


29. Hiller R, Kahn HA. Blindness from glaucoma. Am J Ophthalmol. 1975;80:62–9.


30. Sorsby A. The incidence and causes of blindness in England and Wales, 1963–1968. Report on public health and medical subjects No. 128. London: Her Majesty’s Stationery Office; 1972.


31. Leibowitz HM, Krueger DG, Munder LR, et al. The Framingham Eye Study. Surv Ophthalmol. 1980;24(Suppl.):335–610.


32. Ghafour IM, Allan D, Foulds W. Common causes of blindness and visual handicap in the West of Scotland. Br J Ophthalmol. 1983;67:209–13.


33. Aclimandos WA, Galloway NR. Blindness in the city of Nottingham (1980–1985). Eye. 1988;2:431–4.


34. Tielsch JM, Sommer A, Witt K, et al. Blindness and visual impairment in an American urban population. Arch Ophthalmol. 1990;108:286–90.

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