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Risk factors

TL;DR — Age dominates: roughly two-thirds of people older than 80 are affected, and 10-year incidence in an Australian cohort aged ≥49 was 36.0% (nuclear), 28.0% (cortical) and 9.1% (PSC) (Chen 2025, PMID 40227658; Kanthan 2008, PMID 17900695). Among modifiable exposures the strongest evidence is for smoking, corticosteroids, diabetes and ultraviolet-B. Smoking shows a dose–response relationship with cataract extraction and is supported by Mendelian randomisation as causal for senile cataract (Lindblad 2005, PMID 15961589; Larsson 2022, PMID 35816897); risk after cessation approaches never-smoker levels within ~10 years for moderate smokers but takes ~20 years for heavier smokers (PMID 15961589). Corticosteroids carry a route-dependent gradient from topical skin (RR 1.43) to oral use for >5 years (3.25, 95% CI 1.39–7.58) (Prokofyeva 2013, PMID 22715900). Cumulative UV-B doubling raised cortical — but not nuclear — cataract risk 1.60-fold (95% CI 1.01–2.64) in Chesapeake Bay watermen (Taylor 1988, PMID 3185661). Type 1 diabetes brings cataract surgery forward by about 20 years (Grauslund 2011, PMID 19764915). Almost none of this literature is randomised, and confounding by general health behaviour is the standing limitation.

Age and the competing-risk frame

Age is not simply the largest risk factor; it is the axis on which all others act. The human lens grows throughout life so its core accumulates post-translational modification for longer than any other tissue compartment, and a transport barrier around the nucleus develops in the fourth decade (Michael 2011, PMID 21402586). Empirically, incidence of every cataract subtype rose with age (P < 0.0001 for each) over 10 years in the Blue Mountains Eye Study, where 17.8% of the cohort underwent surgery and mean age at surgery was 75.8 years (PMID 17900695). Because cataract surgery is common and mortality in the same age band is high, incidence studies that do not adjust for the competing risk of death understate lifetime risk: in the type 1 diabetes cohort below, the crude 25-year cumulative incidence of cataract surgery was 20.8% but the mortality-adjusted incidence was 29.4% (95% CI 25.6–33.1) (PMID 19764915).

Sex is an independent factor after age adjustment. Women had higher 10-year incidence than men for nuclear (P = 0.04), cortical (P = 0.007), any cataract (P = 0.0006) and cataract surgery (P = 0.03) (PMID 17900695), and women carry 60% of global cataract blindness (Vision Loss Expert Group 2024, PMID 38461217).

Quantified associations

Exposure Effect estimate (95% CI) Population / design Source
Former smoking RR 3.75 (2.26–6.21) European literature review, Caucasian populations aged 40–95 Prokofyeva 2013, PMID 22715900
Current smoking RR 2.34 (1.07–5.15) same PMID 22715900
Smoking intensity Significant dose–response for cataract extraction (P for trend 0.02 current, 0.0002 past) 34,595 Swedish women, 2,128 extractions, prospective Lindblad 2005, PMID 15961589
Genetic liability to smoking Associated with increased risk of senile cataract Meta-analysis of 29 MR studies plus 123 de novo MR analyses Larsson 2022, PMID 35816897
Diabetes duration >10 years RR 2.72 (1.72–4.28) European review PMID 22715900
Asthma or chronic bronchitis RR 2.04 (1.04–3.81) same PMID 22715900
Cardiovascular disease RR 1.96 (1.22–3.14) same PMID 22715900
Oral corticosteroid >5 years RR 3.25 (1.39–7.58) same PMID 22715900
Corticosteroid — parenteral / inhaled / nasal / ear / skin 1.56 (1.34–1.82) / 1.58 (1.46–1.71) / 1.33 (1.21–1.45) / 1.31 (1.19–1.45) / 1.43 (1.36–1.50) same PMID 22715900
Chlorpromazine ≥90 days at ≥300 mg RR 8.8 (3.1–25.1) same PMID 22715900
Doubling of cumulative ocular UV-B OR 1.60 (1.01–2.64) for cortical cataract; no association with nuclear cataract or UV-A 838 Chesapeake Bay watermen, cross-sectional with modelled lifetime dose Taylor 1988, PMID 3185661
Upper vs lowest quartile annual UV-B OR 3.30 (0.90–9.97) same PMID 3185661
Type 1 diabetes 25-y cumulative incidence of cataract surgery 20.8% crude / 29.4% (25.6–33.1) mortality-adjusted; surgery ~20 years earlier than non-diabetic persons 727-patient population-based Danish cohort, 25-y registry follow-up Grauslund 2011, PMID 19764915
Baseline age in type 1 diabetes HR 1.89 per 10 years (1.46–2.27) same PMID 19764915
Diabetic maculopathy HR 1.89 (1.05–3.40) for cataract surgery same PMID 19764915
Cannabis use ≥11 times Cataract diagnosed 4–5 years younger than never-users UK Biobank cross-sectional, ICD-10 H25 Lehrer 2022, PMID 35093261

The Danish diabetes cohort is instructive for what it did not find: duration of diabetes, sex, glycaemic regulation, proteinuria, smoking, blood pressure and retinopathy level were all non-significant predictors of cataract surgery in multivariate analysis (PMID 19764915). Univariable associations reported elsewhere for glycaemic control should therefore be treated cautiously.

Ultraviolet radiation: strong for cortical, weak for nuclear

Both UV-A and UV-B induce cataract experimentally, and the causal relationship is established in animal and in vitro work even though the pathogenetic pathways are incompletely mapped (Löfgren 2017, PMID 27260484; Roberts 2011, PMID 21617534). Epidemiologically the signal is type-specific: the Chesapeake Bay watermen study found a UV-B association with cortical opacity only, and watermen with cortical opacities had 21% higher average annual UV-B exposure (t = 2.23, P = 0.03) (PMID 3185661). Geographic and Medicare-based analyses reach the same conclusion by a different route, identifying latitude and ambient exposure as predictors of cataract surgery after adjustment for age, sex, race, income and eye-care supply (Javitt 1994, PMID 7634999). Reviews of the epidemiological evidence base note that measurement of individual ocular dose — rather than ambient irradiance — is the persistent methodological weakness (Dolin 1994, PMID 8060933; Midelfart 2005, PMID 16396640).

Practical implications are unusually concrete: because reflected UV enters around the edge of spectacles, wraparound sunglasses blocking below 400 nm and UV-absorbing contact lenses are the interventions with a mechanistic rationale (PMID 21617534). The WHO/ILO joint methodology is developing formal estimates of the cataract disability-adjusted life years attributable to occupational solar UV exposure, with a protocol specifying ≥30 J/m²/day at the ocular surface as the exposure definition (Tenkate 2019, PMID 30737039). Occupational reviews rank UV as having strong evidence, while ionising radiation, welding fume, polyaromatic hydrocarbons and tobacco dust are only suggestive (Iwundu 2024, PMID 39850981).

Diabetes and metabolic disease

Diabetic cataract is both more frequent and earlier. Mechanistically it adds a hyperglycaemia-specific route — aldose reductase flux through the polyol pathway with sorbitol accumulation and osmotic stress, plus glycation and oxidative injury — on top of the age-related route (Mishra 2023, PMID 37322647; Kiziltoprak 2019, PMID 30891150; Caird 1964, PMID 14171096). The clinical consequence is not only earlier surgery but a higher-risk operation and a higher-risk retina: diabetic patients face diabetic macular oedema, postoperative macular oedema, retinopathy progression and posterior capsule opacification (PMID 30891150). See surgery with coexisting eye disease.

Cataract is also associated with hypertension, obesity, chronic kidney disease and autoimmune disease, and is a hallmark of numerous metabolic disorders and syndromes; myopia and race appear as non-modifiable factors alongside age and sex (Ang 2021, PMID 33426783). The mechanistic account for axial myopia is now reasonably specific — vitreous liquefaction, excess reactive oxygen species, impaired antioxidant defence and chronic intraocular inflammation producing earlier nuclear and PSC cataract (Świerczyńska 2025, PMID 39813957).

Drugs

Beyond corticosteroids, pharmacovigilance data give a broad but low-specificity map. Analysis of 54,800 FAERS reports (Q1 2004 – Q3 2024), restricted to 2,336 cases involving 691 drugs in people aged 0–45, identified 24 drugs with disproportional cataract signals; the strongest were difluprednate (BCPNN 7.83), prednisolone (6.84) and erdafitinib (5.44), with glucocorticoids, insulin analogues, nitisinone and ranibizumab prominent. Median onset was 74 days for difluprednate and 141 days for prednisolone; antineoplastic agents had the longest average onset (533.89 days) (Hong 2025, PMID 40707607). Disproportionality signals are hypothesis-generating: they carry no denominator, and reporting is confounded by indication — insulin appears because diabetes causes cataract, not necessarily because insulin does.

Statins have been proposed as protective, but the claim rests on observational analyses and remains contested in the correspondence literature (Kostis 2016, PMID 26851145).

Alcohol, nutrition and socioeconomic confounding

Alcohol findings are inconsistent across epidemiological studies and the pathophysiological mechanism is not established; the practical recommendation from the review literature is that drinking history be recorded, not that a threshold be advised (Hiratsuka 2009, PMID 20443769). Dietary associations are numerous and consistently modest: a systematic review of 24 articles reported protective associations for several dietary patterns and for fruit, vegetable, legume and nut intake (Falkowska 2023, PMID 37960238), and vitamin E showed pooled RR 0.73 (95% CI 0.58–0.92) for dietary intake and 0.77 (0.66–0.91) for high serum tocopherol — but only 0.92 (0.78–1.07), non-significant, for supplemental intake, with a non-linear dose–response (Zhang 2015, PMID 25591715). That split between dietary and supplemental estimates is the classic signature of confounding by health behaviour, and it is exactly what the randomised evidence found: high-dose vitamins C and E plus beta-carotene did not affect lens opacity progression or cataract surgery in 4,757 AREDS participants (AREDS Research Group 2001, PMID 11594943).

Socioeconomic status appears as a modifiable factor in reviews (PMID 33426783), but it is inseparable from smoking, nutrition, occupational UV exposure and access to care, and no analysis in this evidence set decomposes it.

Interpreting cataract risk-factor epidemiology

Classic methodological reviews of this literature make three points that still apply. Cataract does not fit a one-exposure-one-outcome model — a component-cause framework is more realistic, and different component causes act on different aetiologic branches (nuclear, PSC, mixed). Age, trauma and intraocular inflammation are unambiguously important but are either inevitable or contribute little population-attributable risk. Undernutrition is the risk factor with the strongest combination of coherence and predictive performance that is also alterable (Hodge 1995, PMID 8654515).

Four practical cautions follow:

  • Type-specific analysis is mandatory. UV-B associates with cortical but not nuclear cataract (PMID 3185661); steroids with PSC (Kačmař 2019, PMID 31238690). Pooling types dilutes real effects and creates spurious ones.
  • Surgery is not cataract. Many cohorts use cataract extraction as the endpoint, which is a compound of lens opacity, access to services, comorbidity and patient preference (PMID 15961589; PMID 19764915).
  • Reverse causation and indication bias. Drug–cataract signals in spontaneous-reporting data are uninterpretable without indication-matched comparators (PMID 40707607).
  • Randomised evidence exists only for supplements, and it is negative (PMID 11594943).

Open questions

  • What is the population-attributable fraction of modifiable exposures? Effect estimates exist for smoking, steroids, UV and diabetes (PMID 22715900; PMID 3185661; PMID 19764915), but no study has combined them into a type-specific attributable-fraction estimate for a defined population, so the achievable prevention ceiling is unknown.
  • Does occupational UV protection reduce cataract incidence? Mechanistic and observational evidence is strong (PMID 3185661; PMID 27260484), the WHO/ILO burden estimate is in progress (PMID 30737039), and yet as of 2026-08-31 no randomised or quasi-experimental evaluation of an eye-protection programme with cataract incidence as the endpoint was identified in the searches behind this page.
  • Is the diabetes effect glycaemia-dependent? The polyol mechanism predicts a glycaemic dose–response (PMID 37322647), but glycaemic regulation was not a significant predictor of cataract surgery in a 25-year type 1 diabetes cohort (PMID 19764915); the discrepancy between mechanism and cohort evidence is unresolved.
  • Do inhaled and topical corticosteroids carry meaningful absolute risk? Relative risks are modest but precise (inhaled 1.58, 1.46–1.71; skin 1.43, 1.36–1.50) (PMID 22715900); the absolute excess in patients requiring long-term therapy — the number that would change prescribing — has not been published in this evidence set.
  • Is the female excess biological or social? Higher age-adjusted incidence in women (PMID 17900695) coexists with lower effective surgical coverage in women (PMID 38461217); no analysis separates the two contributions.

References

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