Particulate matter modifies the association between airborne pollen and daily medical consultations for pollinosis in Tokyo

Konishi, Shoko; Ng, Chris Fook Sheng; Stickley, Andrew; Nishihata, Shinichi; Shinsugi, Chisa; Ueda, Kayo; Takami, Akinori; Watanabe, Chiho

doi:10.1016/j.scitotenv.2014.08.045

Cited by 35 publications

(23 citation statements)

References 49 publications

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“…Several studies have demonstrated epidemiological data that show a correlation between air pollution and the prevalence of asthma and allergies [8,30,31,32]. However, the nasal mucosa air-liquid interface is not suitable as a test system for allergic diseases, since allergies are complex reactions involving epithelial cells, dendritic cells within the subepithelial tissue and perivascular/intranodular lymphocytes.…”

Section: Discussionmentioning

confidence: 99%

The Proinflammatory Potential of Nitrogen Dioxide and Its Influence on the House Dust Mite Allergen Der p 1

Koehler

Paulus

Ginzkey

et al. 2016

Int Arch Allergy Immunol

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Asthma and allergies are both major global health problems with an increasing prevalence, and environmental data implicate an influence of air pollutants on their development. The present study focuses on the influence of nitrogen dioxide (NO₂) and the major allergen of the house dust mite Der p 1 on human nasal epithelial cells of nonallergic patients in vitro. Nasal epithelial mucosa samples of 11 donors were harvested during nasal air passage surgery and cultured as an air-liquid interface. Exposure to 0.1, 1 and 10 ppm NO₂ or synthetic air as a control was performed for 1 h. Subsequently, the cells were exposed to Der p 1 for 24 h. The release of interleukin (IL)-6 and IL-8 was measured by ELISA, and the production of IL-6 mRNA and IL-8 mRNA was measured by RT-PCR. NO₂ exposure resulted in a concentration-dependent release of IL-6, but not IL-8 release. The coexposure of 0.1 ppm NO₂ and Der p 1, or 1 ppm NO₂ and Der p 1 significantly increased both IL-6 and IL-8 release. Exposure to NO₂, Der p 1, or their combination, did not significantly influence the production of IL-6 or IL-8 mRNA. In conclusion, NO₂ increases the release of inflammatory cytokines in human nasal epithelial cells, especially in coexposure with Der p 1, as a mechanism of allergotoxicology.

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Section: Discussionmentioning

confidence: 99%

The Proinflammatory Potential of Nitrogen Dioxide and Its Influence on the House Dust Mite Allergen Der p 1

Koehler

Paulus

Ginzkey

et al. 2016

Int Arch Allergy Immunol

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“…The pollutants are correlated to each other and associated with synergistic effect on human health (WHO 2003;Mauderly and Samet 2009;Konishi et al 2014). The pollutants are correlated to each other and associated with synergistic effect on human health (WHO 2003;Mauderly and Samet 2009;Konishi et al 2014).…”

Section: Pm Concentration Datamentioning

confidence: 99%

Burden of disease attributed to ambient PM2.5 and PM10 exposure in 190 cities in China

Maji

Arora

Dikshit

2017

Environ Sci Pollut Res

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Particulate air pollution is becoming a serious public health concern in urban cities of China. Association of disability-adjusted life years (DALYs) and economic loss with air pollution-related health effects demand quantitative analysis for correctional measures in air quality. This study applies an epidemiology-based exposure-response function to obtain the quantitative estimate of health impact of particulate matter PM and PM across 190 cities of China during years 2014-2015. The annual average concentration of PM and PM is 57 ± 18 μg/m (ranging from 18 to 119 μg/m) and 97.7 ± 34.2 μg/m (ranging from 33.5 to 252.8 μg/m), respectively. Based on the present study, the total estimated annual premature mortality due to PM is 722,370 [95% confidence interval (CI) = 322,716-987,519], 79% of which accounts for adult cerebrovascular disease (stroke) and ischemic heart disease (IHD). The premature mortality in megacities is very high, such as Chongqing (25,162/year), Beijing (19,702/year), Shanghai (19,617/year), Tianjin (13,726/year), and Chengdu (12,356/year). PM pollution has caused 1,491,774 (95% CI = 972,770-1,960,303) premature deaths (age >30) in China. Further, 3,614,064 cases of chronic bronchitis (CB); 13,759,894 cases of asthma attack among all ages; 191,709 COPD-related hospital admission (HA) cases; 499,048 respiratory-related HA; 357,816 cerebrovascular HA; and 308,129 cardiovascular-related HA due to PM pollution have been estimated during 2014-2015. Chongqing, Beijing, Baoding, Tianjin, and Shijiazhuang are the top five contributors to pollution-related mortality, accounting for 3.10, 2.71, 2.49, 2.20, and 2.02%, respectively, of the total deaths caused by PM pollution. The total DALYs associated with PM and PM pollution in China is 7.2 and 20.66 million in 2014-2015, and mortality and chronic bronchitis shared about 93.3% of the total DALYs for PM. During this period, the economic cost of health impact due to PM is approximately US$304,122 million, which accounts for about 2.94% of China's gross domestic product (GDP). Megacities are expected to contribute relatively more to the total costs. The present methodology could be used as a tool to help policy makers and pollution control board authorities, to further analyze costs and benefits of air pollution management programs in China.

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“…The nasal mucosa may also be a major target for many inhaled toxicants in air pollution. Recently, epidemiological studies have demonstrated that exposure to PM 2.5 leads to contact with nasal mucosa, which causes nasal inflammation [4] and exacerbates allergic rhinitis [5]. …”

Section: Introductionmentioning

confidence: 99%

PM2.5-Induced Oxidative Stress and Mitochondrial Damage in the Nasal Mucosa of Rats

Guo

Hong

Dong

et al. 2017

IJERPH

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Exposure to PM2.5 (particulate matter ≤2.5 μm) increases the risk of nasal lesions, but the underlying mechanisms, especially the mechanisms leading to mitochondrial damage, are still unclear. Thus, we investigated the in vivo effects of PM2.5 exposure on the inflammatory response, oxidative stress, the enzyme activities of Na+K+-ATPase and Ca2+-ATPase, and the morphology and function of mitochondria in the nasal mucosa of rats. Exposure to PM2.5 occurred through inhalation of a PM2.5 solution aerosol. The results show that the PM2.5 exposure induced increased levels of malondialdehyde (MDA) and levels of proinflammatory mediators, including interleukin 6 (IL-6), IL-8, and tumor necrosis factor-α (TNF-α). These changes were accompanied by decreases in the activities of total superoxide dismutase (T-SOD), Na+K+-ATPase, and Ca2+-ATPase in rat nasal mucosa. PM2.5 significantly affected the expression of specific mitochondrial fission/fusion genes (OPA1, Mfn1, Fis1, and Drp1) in nasal mucosa. These changes were accompanied by abnormal alterations of mitochondrial structures, including mitochondrial swelling, cristae disorder, and even fission resulting from higher doses of PM2.5. Our data shows that oxidative damage, inflammatory response, and mitochondrial dysfunction may be the toxic mechanisms that cause nasal lesions after exposure to PM2.5.

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Particulate matter modifies the association between airborne pollen and daily medical consultations for pollinosis in Tokyo

Cited by 35 publications

References 49 publications

The Proinflammatory Potential of Nitrogen Dioxide and Its Influence on the House Dust Mite Allergen Der p 1

The Proinflammatory Potential of Nitrogen Dioxide and Its Influence on the House Dust Mite Allergen Der p 1

Burden of disease attributed to ambient PM2.5 and PM10 exposure in 190 cities in China

PM2.5-Induced Oxidative Stress and Mitochondrial Damage in the Nasal Mucosa of Rats

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