In the present report, we performed a time series analysis of the effects of air pollution on the incidence of acute urticaria and chronic urticaria in Shenyang, China, from 2016–2018. Over this time frame, the daily mean concentrations of PM2.5, PM10, and SO2 were almost twice as high as levels outlined in WHO guidelines, indicating that additional focus on the air pollution situation in Shenyang is necessary. We found that acute urticaria and chronic urticaria-related outpatient visits exhibited a seasonal pattern, occurring more frequently in the summer relative to the winter, consistent with trends in O3 levels, although the opposite trend was observed for PM2.5, PM10, and SO2 concentrations.
Shenyang is a heavy industrial city in northeastern China that experiences cold winters. Air pollution sources in this region include vehicle exhaust, industrial emissions, construction site dust emission, and coal combustion. Overall, daily air pollutant concentrations were relatively stable with peak levels in the winter, likely because coal is the primary source of energy and heat during the colder months, and because lower temperatures are not conducive to air pollutant dispersal. In contrast, O3 levels were higher during the summer, consistent with the intense solar radiation and higher temperatures during this season, which can increase photochemical reaction intensity and O3 concentrations near the surface.
Rates of dermatosis are rising, and epidemiological studies suggest that short-term exposure to ambient air pollution can cause adverse effects on skin health (Ahn 2014, Kathuria &Silverberg 2016, Kramer et al. 2009, Li et al. 2015, Schafer et al. 1996, Suarez-Varela et al. 2013, Vierkotter et al. 2010). Herein, we found that exposure to three air pollutants (PM2.5, PM10, and O3) significantly increased the risk of urticaria outpatient visits, with evidence of cumulative lag effects following such exposure. The impact of O3 on acute urticaria was more significant than that on chronic urticaria, with the cumulative lag effect of O3 exposure only remaining significant on 1 and 2 days post-exposure for acute urticaria outpatient visits. We observed no relationship between SO2 exposure and urticaria outpatient visits. Our findings were similar to those of a study conducted in Shanghai, which found that elevated ground O3 levels were associated with increased numbers of emergency medical visits for urticaria, eczema, contact dermatitis, and infectious skin diseases, whereas there was no significant relationship between these conditions and exposure to PM10, NO2 and SO2 (Xu et al.). In another study conducted in Korea, Lee et al. determined that increases in daily mean O3 concentrations were linked to increased hospitalization rates for patients with asthma and atopic dermatitis (Lee et al. 2010).
Many environmental pollutants have been shown to cause direct oxidative damage, including NO2 and O3, which can catalyze reactive oxygen species (ROS) production that can disrupt cutaneous redox homeostasis and cause skin cell damage (Cotovio et al. 2001, Ghio et al. 2012). Exposure to a range of O3 concentrations can alter levels of IgE specific for plant pollen in humans (Beck et al. 2013, Garcia-Gallardo et al. 2013, Rogerieux et al. 2007). The sensitivity of the human body to such O3 exposure is both dose- and allergen-specific. Exposure to high levels of O3 on a daily basis may thus drive the incidence of urticaria, asthma, and other allergic diseases. In summary, exposure to lower levels of O3 during warmer seasons may reduce the incidence of urticaria, although further research is necessary to confirm this hypothesis.
Particulate matter is primarily derived from vehicle and industrial exhaust sources, and is primarily composed of aromatic hydrocarbons and other organic compounds that can activate diverse biological processes and drive ROS production (Furue et al. 2014). ROS-mediated oxidative stress is thought to be linked to the pathogenesis of urticaria and other dermatological conditions ( Kalkan et al. 2014). Previous studies have suggested that exposure to PM2.5 and PM10 is linked to higher rates of acne vulgaris and atopic dermatitis in adults and children (Kathuria &Silverberg 2016, Kramer et al. 2009, Yunquan et al. 2016). Interestingly, we found that PM2.5 exposure was associated with stronger cumulative effects on chronic urticaria incidence relative to PM10 exposure. Certain epidemiological analyses of PM exposure have linked the exposure to these pollutants to skin inflammatory response processes associated with dermatitis, acne, and psoriasis (Liu et al. 2018, Song et al. 2011, Tsuji et al. 2011, Yang et al. 2014).
While the mechanistic basis for our findings remains to be clarified, they are consistent with the result of a few prior studies. For example, Ono et al. found that polycyclic aromatic hydrocarbons (PHAs) in air organic pollutants can attach to the skin and cause damage thereto. The activation of aryl hydrocarbon receptor (AhR) signaling in keratinocytes can drive the production of inflammatory cytokines including IL-6 and IL-8 (Ono et al. 2013). Researchers have also shown that metals on the surface of PM can additionally drive ROS production, lipid oxidation, and skin cell apoptosis in a dose-dependent manner (Lefebvre et al. 2016).
There are several limitations to this analysis. For one, this was a large-scale population-based study without any analyses of patients at the individual level, potentially introducing aggregation bias. In addition, Shengjing Hospital is a general hospital with a higher number of children as patients relative to other hospitals in this region. This may have increased the overall proportion of children in the study population. Differences in climate characteristics, air pollution composition, and personal behaviors may also limit the applicability of these findings to similar analyses conducted in other regions.