ry eye is a multifactorial chronic disease of the tears and ocular surface. 1 Worldwide, the prevalence of dry eye ranges from 5% to 50% and varies owing to population characteristics, disease definition, and other risk factors. 2 In the United States, approximately 16.4 million adults (6.8%) have been diagnosed with dry eye. 3 Symptoms of dry eye are heterogeneous and include painful symptoms (ie, dryness, burning, irritation) and vision-related symptoms (ie, poor or fluctuating vision), which can negatively affect physical health, mental health, and quality of life. 2 Signs of dry eye are likewise heterogeneous and include decreased tear production, increased tear evaporation, inflammation, and high tear osmolarity. 4 Numerous risk factors for dry eye have been iden-tified, including age, sex, comorbidities such as depression and arthritis, and medications such as antihistamines. 2 Dry eye is also influenced by environmental factors, including wind, 5 high temperature, 6 low humidity, 5 high altitude, 7 and air pollution. 5 In a study of 500 hospital-based individuals in India, 6 wind and high temperature exposure, as assessed by self-report, correlated with dry eye prevalence (odds ratios, 2.15 and 1.91, respectively). In a study of 3.41 million US veterans, the risk of a diagnosis of dry eye was 6% and 7% higher in zip codes where wind speed and humidity were 1 SD less than the mean, respectively. The risk of a dry eye diagnosis was also 13% higher in zip codes where aerosol optical depth, a measure of atmospheric aerosols that include air-IMPORTANCE The ocular surface is continuously exposed to the environment. Although studies have focused on associations between outdoor environmental conditions and dry eye, information on associations between the indoor environment and dry eye is lacking.OBJECTIVE To determine associations between the indoor environment and dry eye. DESIGN, SETTING, AND PARTICIPANTSThis prospective cross-sectional study sample of 97 veterans with a wide range of dry eye metrics was recruited from the Miami Veterans Affairs Healthcare eye clinic from October 19, 2017, to August 30, 2018. Dry eye metrics were first evaluated in the clinic, followed by indoor home environmental metrics within 1 week using a handheld particle counter. Data were analyzed from October 19, 2017, to August 30, 2018.MAIN OUTCOMES AND MEASURES Symptoms of dry eye were assessed with standardized questionnaires. Dry eye signs were assessed via standard examination. Indoor environmental metrics included temperature, humidity, and particulate matter mass and count. RESULTSOf the 97 participants included in the analysis, 81 (84%) were men, with a mean (SD) age of 58.2 (11.9) years. Dry eye symptoms were in the moderate range with a mean (SD) Ocular Surface Disease Index (OSDI) score of 31.

BACKGROUND Penetrating traumatic brain injury induces chronic inflammation that drives persistent tissue loss long after injury. Absence of endogenous reparative neurogenesis and effective neuroprotective therapies render injury-induced disability an unmet need. Cell replacement via neural stem cell transplantation could potentially rebuild the tissue and alleviate penetrating traumatic brain injury disability. The optimal transplant location remains to be determined. METHODS To test if subacute human neural stem cell (hNSC) transplant location influences engraftment, lesion expansion, and motor deficits, rats (n = 10/group) were randomized to the following four groups (uninjured and three injured): group 1 (Gr1), uninjured with cell transplants (sham+hNSCs), 1-week postunilateral penetrating traumatic brain injury, after establishing motor deficit; group 2 (Gr2), treated with vehicle (media, no cells); group 3 (Gr3), hNSCs transplanted into lesion core (intra); and group 4 (Gr4), hNSCs transplanted into tissue surrounding the lesion (peri). All animals were immunosuppressed for 12 weeks and euthanized following motor assessment. RESULTS In Gr2, penetrating traumatic brain injury effect manifests as porencephalic cyst, 22.53 ± 2.87 (% of intact hemisphere), with p value of <0.0001 compared with uninjured Gr1. Group 3 lesion volume at 17.44 ± 2.11 did not differ significantly from Gr2 (p = 0.36), while Gr4 value, 9.17 ± 1.53, differed significantly (p = 0.0001). Engraftment and neuronal differentiation were significantly lower in the uninjured Gr1 (p < 0.05), compared with injured groups. However, there were no differences between Gr3 and Gr4. Significant increase in cortical tissue sparing (p = 0.03), including motor cortex (p = 0.005) was observed in Gr4 but not Gr3. Presence of transplant within lesion or in penumbra attenuated motor deficit development (p < 0.05) compared with Gr2. CONCLUSION In aggregate, injury milieu supports transplanted cell proliferation and differentiation independent of location. Unexpectedly, cortical sparing is transplant location dependent. Thus, apart from cell replacement and transplant mediated deficit amelioration, transplant location–dependent neuroprotection may be key to delaying onset or preventing development of injury-induced disability. LEVEL OF EVIDENCE Preclinical study evaluation of therapeutic intervention, level VI.