“…A South Korean study of 41 children aged 8-12 years collected symptom diaries for 67 days and found significant associations between pruritus severity and daily ambient PM concentrations [103]. A longer term study of 22 Korean children using symptom diaries for 18 months also found associations of AD symptoms with levels of outdoor air pollutants [104].…”
Introduction-The etiology of atopic dermatitis (AD) is multifactorial with interaction between genetics, immune and environmental factors.Areas covered-We review the role of prenatal exposures, irritants and pruritogens, pathogens, climate factors, including temperature, humidity, ultraviolet radiation, outdoor and indoor air pollutants, tobacco smoke exposure, water hardness, urban vs. rural living, diet, breastfeeding, probiotics and prebiotics on AD.Expert commentary-The increased global prevalence of AD cannot be attributed to genetics alone, suggesting that evolving environmental exposures may trigger and/or flare disease in predisposed individuals. There is a complex interplay between different environmental factors, including individual use of personal care products and exposure to climate, pollution, food and other exogenous factors. Understanding these complex risk factors is crucial to developing targeted interventions to prevent the disease in millions. Moreover, patients require counseling on optimal regimens for minimization of exposure to irritants and pruritogens and other harmful exposures.
“…A South Korean study of 41 children aged 8-12 years collected symptom diaries for 67 days and found significant associations between pruritus severity and daily ambient PM concentrations [103]. A longer term study of 22 Korean children using symptom diaries for 18 months also found associations of AD symptoms with levels of outdoor air pollutants [104].…”
Introduction-The etiology of atopic dermatitis (AD) is multifactorial with interaction between genetics, immune and environmental factors.Areas covered-We review the role of prenatal exposures, irritants and pruritogens, pathogens, climate factors, including temperature, humidity, ultraviolet radiation, outdoor and indoor air pollutants, tobacco smoke exposure, water hardness, urban vs. rural living, diet, breastfeeding, probiotics and prebiotics on AD.Expert commentary-The increased global prevalence of AD cannot be attributed to genetics alone, suggesting that evolving environmental exposures may trigger and/or flare disease in predisposed individuals. There is a complex interplay between different environmental factors, including individual use of personal care products and exposure to climate, pollution, food and other exogenous factors. Understanding these complex risk factors is crucial to developing targeted interventions to prevent the disease in millions. Moreover, patients require counseling on optimal regimens for minimization of exposure to irritants and pruritogens and other harmful exposures.
“…45 For 67 consecutive days, daily symptom scores were recorded, and daily PM concentrations were measured on the rooftop of the school building. By using linear regression analysis, it was found that the itching score was significantly associated with the concentrations of ambient ultrafine particles with a diameter less than 0.1 mm but not of larger particles, after adjustment for confounding factors, such as age, sex, height, SCORAD index, commuting time, and temperature.…”
Section: Air Pollutants Associated With Aggravation Of Admentioning
“…Recently, the effect of PM 2.5 on the skin has attracted attention of both clinical dermatologists and basic scientists (Han et al 2016; Li et al 2017), who recognized ambient PM 2.5 as a crucial risk factor in skin diseases. Thus, PM 2.5 was shown to aggravate symptoms in children with allergic dermatitis and eczema (Song et al 2011), and to promote inflammatory disorders, aging, androgenetic alopecia, and cancers of the skin (Kim et al 2016). …”
The skin is the largest organ of the human body and the one mostly exposed to outdoor contaminants. To evaluate the biological mechanisms underlying skin damage caused by fine particulate matter (PM2.5), we analyzed the effects of PM2.5 on cultured human keratinocytes and the skin of experimental animals. PM2.5 was applied to human HaCaT keratinocytes at 50 µg/mL for 24 h and to mouse skin at 100 µg/mL for 7 days. The results indicate that PM2.5 induced oxidative stress by generating reactive oxygen species both in vitro and in vivo, which led to DNA damage, lipid peroxidation, and protein carbonylation. As a result, PM2.5 induced endoplasmic reticulum stress, mitochondrial swelling, and autophagy, and caused apoptosis in HaCaT cells and mouse skin tissue. The PM2.5-induced cell damage was attenuated by antioxidant N-acetyl cysteine, confirming that PM2.5 cellular toxicity was due to oxidative stress. These findings contribute to understanding of the pathophysiological mechanisms triggered in the skin by PM2.5, among which oxidative stress may play a major role.
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