Wang et al. report the association between risk of POAG and lead exposure (which leads to oxidative stress) using bone lead as a biomarker of cumulative lead dose (tibia lead) or an endogenous source of stored lead (patella lead). The study examined a prospective cohort of 634 men without glaucoma who had tibia and patella K X-ray fluorescence lead measurements between 1991 and 1999 and standard ocular evaluations by optometrists until end of 2014. Forty-four incident cases of POAG were identified by the end of follow-up (incidence rate = 74 per 10,000 person-years; median follow-up = 10:6 y) and a ten-fold increases in patella lead and tibia lead were associated with HRs of 5.06 (95% CI: 1.61, 15.88, p = 0:005) and 3.07 (95% CI: 0.94, 10.0, p = 0:06), respectively. This study provides the first longitudinal evidence that increased levels of bone lead may be an important risk factor for POAG.
This study provides the first longitudinal evidence that increased levels of bone lead may be an important risk factor for POAGThe major limitations of the study are the nonspecific criteria for diagnosis of glaucoma and the diagnosis not being confirmed by glaucoma specialists. Glaucoma (POAG) was diagnosed by optometrists in participants who showed any one of the following characteristics: (a) either eye having a CDR ≥ 0.7; (b) the difference of two eyes' CDRs ≥ 0:2; (c) any eye's CDR ≥ 0:6, with either disc hemorrhage or visual field defect; or (d) vision loss due to nerve fiber layer loss. This could have led to an overestimation of glaucoma with incorporation of false positive results based on large cup disc ratio's (physiological cupping) and nerve fiber layer loss due to causes of optic atrophy other than glaucoma. Longitudinal evaluation with serial photographs of the optic nerve and evaluation by expert ophthalmologists to detect structural changes were missing. Additionally, the IOP levels after follow-up were not included. It would have been useful if the investigators documented IOP values during follow-up and produced evidence for elevation of IOP attributed to lead toxicity which subsequently caused the development of glaucoma. Furthermore, eyes which were later diagnosed as POAG had much higher rates of ocular hypertension at baseline as compared to those who did not develop glaucoma (18.2 vs 2.2%) and this raises a possibility that all subjects were not free of glaucoma at baseline evaluation. Data on impact of lead toxicity on other systems which may seriously impact quality of life and also impact glaucoma such as central/peripheral nervous system, cardiovascular, gastrointestinal, renal, haematological, etcetera, and blood levels of lead to categorize severity of health risk at baseline/ follow-up were also not incorporated.
Nevertheless, the manuscript presents a valuable addition to published literature and underscores the importance of evaluating POAG patients (especially with occupational exposure) for lead toxicity.