Air pollution is an important public health concern. According to the World Health Organization, most significant constituents of air pollution include particulate matter (PM), ozone, nitrogen dioxide, and sulfur dioxide.¹ The main sources of PM and nitrogen dioxide are vehicles and the burning of fuels.² Ozone is formed in the atmosphere by photochemical reactions that occur as a result of the action of UV light on precursor pollutants, such as the oxides of nitrogen and volatile organic compounds.¹ Sulfur dioxide is produced from industrial processing of sulfur-containing materials.³ Ambient levels of air pollution are known to be associated with a wide range of adverse health effects that particularly affect the respiratory and cardiovascular systems.^4,5

Dry eye disease (DED) is one of the major ophthalmological healthcare challenges worldwide. DED is a multifactorial disease characterized by a loss of homeostasis of the tear film, and its main pathogenesis is chronic ocular surface inflammation related with various cellular and molecular signaling cascades. The animal model is a reliable and effective tool for understanding the various pathological mechanisms and molecular cascades in DED. Considerable experimental research has focused on developing new strategies for the prevention and treatment of DED. Several experimental models of DED have been developed, and different animal species such as rats, mice, rabbits, dogs, and primates have been used for these models. Although the basic mechanisms of DED in animals are nearly identical to those in humans, proper knowledge about the induction of animal models is necessary to obtain better and more reliable results. Various experimental models (in vitro and in vivo DED models) were briefly discussed in this review, along with pathologic features, analytical approaches, and common measurements, which will help investigators to use the appropriate cell lines, animal, methods, and evaluation parameters depending on their study design.

Background: To evaluate the effects of pretreatment for dry eye disease (DED) on the accuracy of intraocular lens (IOL) power calculation. Methods: Patients who underwent uneventful cataract surgery were included in the study. IOL power was determined using the SRK/T and Barrett Universal II (Barrett) formulas. The patients were divided into non-pretreatment and pretreatment groups, and those in the pretreatment group were treated with topical 0.5% loteprednol etabonate and 0.05% cyclosporin A for 2 weeks prior to cataract surgery. Ocular biometry was performed in all groups within 2 days before surgery. The mean prediction error, mean absolute error (MAE), and proportions of refractive surprise were compared between the non-pretreatment and pretreatment groups at 1 month postoperatively. Refractive surprise was defined as MAE ≥ 0.75D. Results: In a total of 105 patients, 52 (52 eyes) were in the non-pretreatment group and 53 (53 eyes) in the pretreatment group. The MAE was 0.42 ± 0.33, 0.38 ± 0.34 (SRK/T, Barrett) and 0.23 ± 0.19, 0.24 ± 0.19 in the non-pretreatment and pretreatment groups, respectively (p < 0.001/=0.008). The number of refractive surprises was also significantly lower in the pretreatment group. [non-pretreatment/pretreatment: 9/2 (SRK/T); 8/1 (Barrett); p = 0.024/0.016]. Pretreatment of DED was related to a reduction in postoperative refractive surprise. [SRK/T/Barrett: OR = 0.18/0.17 (95% CI: 0.05–0.71/0.05–0.60), p = 0.014/0.006]. Conclusions: The accuracy of IOL power prediction can be increased by actively treating DED prior to cataract surgery.

Lee KW, et al. J Korean Med Sci. 2017 Jan;32(1):143-150. https://doi.org/10.3346/jkms.2017.32.1.143