The Impact Of Climate Factors On Morbidities Of Eczema And The Skin Barrier Function

PART ⅠPurposeEczema is driven by a complex relationship between genetic predisposition and environmental exposures. We sought to determine the impact of specific climatic factors on the prevalence of eczema in Shanghai, China.Patients and MethodsCollected the data of daily outpatient visits to the department of dermatology, Huashan Hospital Affiliated to Fudan University from 2007 to 2011, and climate factors of Shanghai during the same period, including outdoor air temperature, sulfur dioxide, nitrogen dioxide, PM10, PM2.5, ozone and relative humidity. The outpatient diseases were classified using Clinical Dermatology standard. The relationship between eczema and climate factors were statistically analyzed. Generalized additive model (GAM) extended poisson regression was used to examine the exposure-response relationship between various climate factors and the quantity of eczema outpatients from 2007 to 2011.ResultsThe whole number of outpatients was 2683778, in department of dermatology, Huashan Hospital Affiliated to Fudan University, Shanghai, China, from 2007 to 2011, and the number of eczema patients was 510158, with a daily average of 279.4 visits. The climate factors kept stable basically, with the daily mean level of air temperature 17.44℃, relative humidity 58.87%, sulfur dioxide 42.31 μg/m3, nitrogen dioxide 60.22μg/m3,PM10 83.24 μg/m3, PM2.555.62 μg/m3, and ozone 68.99 μg/m3. Correlation analysis showed that eczema outpatients were positively correlated with temperature, sulfur dioxide, nitrogen dioxide and PM10, and inversely correlated with relative humidity. Statistical analysis based on generalized additive Poisson regression model showed that eczema patients would significantly decreased in conditions of elevation of the relative humidity and decreasing of the outdoor temperature and the levels of PM10, SO2 and NO2 (p<0.05), the effect coefficients were -0.4108,0.7180, 0.04535,0.1198 and 0.2505, respectively. And the impact of SO2, NO2, relative humidity and PM10 on eczema outpatients quantity has lag effects.ConclusionsFrom 2007-2011, there are significant and positive correlations between the quantity of eczema outpatients in Shanghai and the level of temperature, PM10, NO2 and SO2, and inverse correlations between the former and relative humidity. The impact of relative humidity, PM10, NO2 and SO2 has some lag effect.PART IIPurposeTo explore the impact of PM2.5 on HaCaT cells and the potential mechanisms.Materials and MethodsHaCaT cells were stimulated with PM2.5 of different concentrations (10 μg/mL,25 μg/mL,50 ug/mL,100 μg/mL and 200 μg/mL). Cellular survival and apoptotic rate were measured by flow cytometry and Cell Counting Kit-8 (CCK-8), and curves for cell survival/inhibition were drawn. After the exposure of PM2.5, The expression of filaggrin, RPTN, loricrin and involucrin were exzamined at the level of mRNA and protein, by RealTime PCR and Western blot, respectively. And the changes of cytokines secreted by HaCaT cells after the stimulation were detected by ELISA, including IL-1α, IL-1β,IL-6, IL-8, TNF-α, GM-CSF and TSLP.ResultsAfter the exposure of different concentrations or the same concentration but different exposing time, the survival rate of HaCaT cells would decrease along with the increasing of the concentrations of PM2.5 and time of exposure. Besides, the apoptotic rate of HaCaT cells detected by flow cytometry increased along with the increasing of PM2.5 concentrations. The expression of Filaggrin and RPTN were elevated when the concentrations of PM2.5 got higher, which were detected by both RealTime PCR and Western blot. GM-CSF、TSLP and TNF-a were also over secreted by HaCaT cells. But the expressions of Loricrin, Involucrin, IL-α, IL-β, IL-6 and IL-8 were not significantly changed.ConclusionsAfter the exposure of PM10, HaCaT cells showed inhibition of cellular survival and increasing of cellular apoptosis. And the expression of filaggrin and RPTN protein and the cytokines such as GM-CSF, TSLP and TNF-a in HaCaT increased.