Pediatric Asthma Attack and Home Paint Exposure.

Although asthma mortality has been declining for the past several decades, asthma morbidity is on the rise, largely due to deteriorating indoor air quality and comorbidities, such as allergies. Consumer products and building materials including paints emit volatile organic compounds (VOCs), such as propylene glycol (PG), which is shown to dehydrate respiratory tracts and can contributor to airway remodeling. We hypothesize that paint exposure increases the risk of asthma attacks among children because high levels of VOCs persist indoors for many weeks after painting. Children 1-15 years old visiting two of the University of Miami general pediatric clinics were screened for their history of asthma and paint exposure by interviewing their parents and/or guardians accompanying them to the clinic. They were also asked questions about asthma diagnosis, severity of asthma and allergies and their sociodemographics. The risk of asthma attack among asthmatic children was modeled with respect to paint exposure adjusting for potential confounders using multivariate logistic regressions. Of 163 children, 36 (22%) reported physician-diagnosed asthma and of these, 13 (33%) had an asthma attack during the last one year. Paint exposure was marginally significant in the univariate analysis (OR = 4.04; 95% CI = 0.90-18.87; p < 0.1). However, exposed asthmatic children were 10 times more likely to experience an asthma attack than unexposed asthmatic children (OR = 10.49; CI = 1.16-94.85, p < 0.05) when adjusted for other risk factors. Given paint is one of the sources of indoor VOCs, multiple strategies are warranted to manage the health effects of VOC exposure from paint, including the use of zero-VOC water-based paint, exposure avoidance and clinical interventions.

Association of the Indoor Environment With Dry Eye Metrics.

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 Participants: This 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. Results: Of 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 31.2 (23.6). Humidity was associated with worse symptoms and signs, including OSDI score (r = 0.30 [95% CI, 0.07-0.49]; P = .01), inflammation (r = 0.32 [95% CI, 0.10-0.51]; P = .01), Schirmer score (r = -0.25 [95% CI, -0.45 to 0.02]; P = .03), eyelid vascularity (r = 0.27 [95% CI, 0.05-0.47]; P = .02), and meibomian gland dropout (r = 0.27 [95% CI, 0.05-0.47]; P = .02). In multivariate analyses, particulate matter of 2.5 µm or less (PM2.5) was associated with dry eye metrics when adjusted for demographic characteristics, comorbidities, medications, and interaction variables. For example, a 1-unit increase in instrumented PM2.5 level was associated with a 1.59 increase in the OSDI score (95% CI, 0.58-2.59; P = .002), a 0.39 reduction in Schirmer score (95% CI, -0.75 to -0.03; P = .04), a 0.07 increase in meibomian gland dropout (95% CI, 0.01-0.13; P = .02), and a 0.06 increase in inflammation (95% CI, 0.02-0.11; P = .009). Conclusions and Relevance: When adjusting for humidity, this study found that increased particulate matter exposure was associated with worse dry eye metrics. Humidity was positively associated with dry eye metrics, potentially because higher humidity increases microbial growth and particulate matter size and mass.

Human neural stem cell transplant location-dependent neuroprotection and motor deficit amelioration in rats with penetrating traumatic brain injury.

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.