June 2020
Volume 61, Issue 7
ARVO Annual Meeting Abstract  |   June 2020
Indoor Carbon Monoxide and Ocular Surface Inflammation
Author Affiliations & Notes
  • Frank Miralles
    Department of Public Health Sciences, University of Miami, Miami, Florida, United States
  • Naresh Kumar
    Department of Public Health Sciences, University of Miami, Miami, Florida, United States
  • Anat Galor
    Bascom Palmer Eye Institute, Miami, Florida, United States
    Ophthalmology, Miami Veterans Administration Medical Center, Miami, Florida, United States
  • Footnotes
    Commercial Relationships   Frank Miralles, None; Naresh Kumar, None; Anat Galor, None
  • Footnotes
    Support  NEI 1R01EY026174-01A1 - 667514
Investigative Ophthalmology & Visual Science June 2020, Vol.61, 398. doi:
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      Frank Miralles, Naresh Kumar, Anat Galor; Indoor Carbon Monoxide and Ocular Surface Inflammation. Invest. Ophthalmol. Vis. Sci. 2020;61(7):398.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose : Although air pollution, such as airborne particulate matter, has been linked to dry eye (DE), the effects of reactive gases such as carbon monoxide (CO) have not been well documented. Given that reactive gases are shown to induce lipid peroxidation and can target the lipid in the outermost layer of the eye’s protective tear film, we hypothesize that CO exposure is associated with DE measures, especially Matrix metallopeptidase 9 (MMP9) levels, a marker of inflammation.

Methods : In this prospective study of 39 unique subjects, 19 seen once and 20 seen twice, in the Miami VA. Each visit involved a comprehensive eye exam to assess DE symptoms and signs. Home air quality monitoring was conducted within a week after each clinical visit. Analysis was restricted to DE signs including measures of ocular surface MMP9 (Inflammadry, Quidel), tear break up time, corneal staining, and tear production via Schirmer strips. A portable instrument was used in the subject’s home to monitor levels of reactive gases, particulate matter, temperature and humidity. Subjects with detectable ocular surface MMP9 were considered cases (MMP9+) and those without detectable MMP9 served as controls (MMP9-). Using logistic regression, odds of MMP9+ was computed against CO exposure (as a continuous and categorical variable), adjusting for potential confounders, such as age, gender and smoking exposure, as well as multiple visits.

Results : During the 59 clinical visits, 21 individuals were found to have detectable MMP+ on the ocular surface. The frequency of MMP+ increased with increasing exposure to CO (χ2 ~ 13.; p ~ 0.001 Table 1; Figure 1). In the multivariate model, one ppm increase in CO exposure was associated with a 5% increased risk of MMP9+ (odds ratio ~ 1.05; 95% CI = 1.019 - 1.085; p < 0.001). When CO concentration was examined categorically (divided into a concentration of > vs ≤ 35ppm based on the EPA hourly threshold), individuals exposed to CO concentrations >35 ppm were 11.4x more likely to have detectable MMP9+ as compared to individuals exposed to CO concentrations ≤ 35ppm (odds ratio ~ 11.; 95% CI = 1.68 - 81.45; p < 0.05). CO exposure was not associated with other DE signs examined.

Conclusions : Our findings suggest that CO exposure is associated with an increased risk of ocular surface inflammation. This study highlights the need to recognize the possible ocular and systemic effects of short- and long-term exposure to environmental reactive gases.

This is a 2020 ARVO Annual Meeting abstract.




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