Ambient air pollutants increase the risk of immunoglobulin E–mediated allergic diseases: a systematic review and meta-analysis

Abstract

Immunoglobulin E (IgE)-mediated allergic diseases, including eczema, atopic dermatitis (AD), and allergic rhinitis (AR), have increased prevalence in recent decades. Recent studies have proved that environmental pollution might have correlations with IgE-mediated allergic diseases, but existing research findings were controversial. Thus, we performed a comprehensive meta-analysis from published observational studies to evaluate the risk of long-term and short-term exposure to air pollutants on eczema, AD, and AR in the population (per 10-μg/m 3 increase in PM 2.5 and PM 10 ; per 1-ppb increase in SO 2 , NO 2 , CO, and O 3 ). PubMed, Embase, and Web of Science were searched to identify qualified literatures. The Cochran Q test was used to assess heterogeneity and quantified with the I 2 statistic. Pooled effects and the 95% confidence intervals (CIs) were used to evaluate outcome effects. A total of 55 articles were included in the study. The results showed that long-term and shortterm exposure to PM 10 increased the risk of eczema (PM 10 , RR long = 1.583, 95% CI: 1.328, 1.888; RR short = 1.006, 95% CI: 1.003-1.008) and short-term exposure to NO 2 (RR short = 1.009, 95% CI: 1.008-1.011) was associated with eczema. Short-term exposure to SO 2 (RR short : 1.008, 95% CI: 1.001-1.015) was associated with the risk of AD. For AR, PM 2.5 (RR long = 1.058, 95% CI: 1.014-1.222) was harmful in the long term, and short-term exposure to PM 10 (RR short : 1.028, 95% CI: 1.008-1.049) and NO 2 (RR short : 1.018, 95% CI: 1.007-1.029) were risk factors. The findings indicated that exposure to air pollutants might increase the risk of IgE-mediated allergic diseases. Further studies are warranted to illustrate the potential mechanism for air pollutants and allergic diseases.

Preventative Effects of Antioxidants against PM10 on Serum IgE Concentration, Mast Cell Counts, Inflammatory Cytokines, and Keratinocyte Differentiation Markers in DNCB-Induced Atopic Dermatitis Mouse Model

“…Air pollution may be related to the development and exacerbation of AD [ 30 , 31 , 32 , 33 ]. Woo et al [ 34 ] reported that PM 10 exposure induces and aggravates skin inflammation via the differential expression of genes controlling skin barrier integrity and immune response in ovalbumin (OVA)-treated mice.…”

Examining the impact of air pollution, climate change, and social determinants of health on asthma and environmental justice

“…This study by Wang et al [11] observed a significant association between long term exposure to PM 2.5 , NO 2 , and CO and the development of allergic rhinitis (AR) and atopic dermatitis (AD). The observation that an increase in NO 2 and CO exposure was associated with a significant elevation in immunoglobulin E (IgE) and subsequent allergic diseases, suggested a potential association with allergic asthma as well [11]. The potential risk of outdoor air pollution is enhanced given the significant contribution of outdoor air pollution to indoor air quality.…”

“…In urban areas, traffic related air pollution (TRAP) is a particular focus. A recent systematic review and meta-analysis evaluated ambient air pollutants and the risk of immunoglobulin E-mediated allergic disease [11]. This study by Wang et al [11] observed a significant association between long term exposure to PM 2.5 , NO 2 , and CO and the development of allergic rhinitis (AR) and atopic dermatitis (AD).…”

Effects of Coarse and Fine Atmospheric Particulate Matter on a Mast Cell Line

“…大気中に浮遊する粒径が 2.5 µm 以下の粒子は， 呼吸器の奥深く肺胞まで到達し，血中への移行を 通じた重篤な健康被害をもたらす．例えば，慢 性 閉 塞 性 肺 疾 患(chronic obstructive pulmonary disease: COPD) 1) などの呼吸器系，院外心原性心停止 (out-of-hospital cardiac arrest: OHCA) 2,3) などの循環 器系及びアレルギー性鼻炎 4) などの免疫系，更に肺 がん 5) のような発がん性など多くの健康影響 [6][7][8] が 報告されている．大気粒子状物質は，発生源から直 接排出される一次粒子［有機炭素(有機化合物) ，元 素状炭素，無機元素(金属)など］と排出時にはガ ス状物質であるが，それらの化学反応により粒子化 される二次生成粒子(硫酸塩，硝酸塩，アンモニウ ム塩，低分子有機酸 9) など)が知られている． [10][11][12] 浮 遊 粒 子 状 物 質(suspended particulate matter: 18,19) その結果，硫酸アンモニウム は，細胞障害性を誘発し， 18) また，細胞障害を引き 起こさない条件で C57 細胞の脱顆粒を誘発，又は thapsigargin の刺激による脱顆粒反応を増強するこ とを報告した． 19) さらに，それらに影響するイオン は，硫酸アンモニウムの構成成分のうち，硫酸イオ ンではなくアンモニウムイオンであることを明らか にした． 18,19) ついで，われわれは中国大陸から PM 2. の培養条件を一部改良して行った．すなわち， ( 1)…”