Exposure to ambient ultrafine particles and urinary 8-hydroxyl-2-deoxyguanosine in children with and without eczema

Song, Sanghwan; Paek, Domyung; Park, Chunghee; Lee, Chul-Woo; Lee, Jung-Hyun; Yu, Seung-Do

doi:10.1016/j.scitotenv.2013.04.011

Cited by 25 publications

(19 citation statements)

References 45 publications

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“…In detail, four studies were published in the 1990s, nine in the 2000s, and 21 in the last decade. Different geographical areas (and ethnicities) were not uniformly represented: 16 studies [17,18,23,24,27,[32][33][34][35][36][37][38]40,42,45,46] were performed in Eastern Asia (8 in Japan, 6 in Korea, 2 in Taiwan), nine [21,28,31,39,41,43,44,47,48] in Europe (3 in Russia, 2 in Germany, 1 in Finland, Italy, Norway, Switzerland), four [20,22,29,30] in Middle Eastern countries (3 in Turkey, 1 in Israel), two [25,26] in Southern Asia (Bangladesh, India), and one [49] in the United States of America. Another study [19] included patients from multiple Canadian and European centers.…”

Section: Resultsmentioning

confidence: 99%

“…Levels of this marker were significantly increased in AD patients compared with healthy controls in three studies [42,45,46]. Conversely, two studies reported no significant differences between patients and controls [27,37], but one of them [27] demonstrated that subjects affected by AD have a significantly higher increase of 8-OHdG after exposure to environmental pollution (ultrafine particles, particle bound polycyclic aromatic hydrocarbons).…”

Section: Biomarkersmentioning

confidence: 96%

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Oxidative Stress and Atopic Dermatitis

et al. 2020

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Atopic dermatitis is a common chronic/chronically relapsing inflammatory skin disease, with increasing worldwide prevalence. Etiopathogenesis is complex and multifactorial, with a mix of genetic, immunological and environmental aspects. Like in other chronic inflammatory diseases, oxidative stress plays an important pathogenetic role. We reviewed in vivo research studies on humans about oxidative stress and atopic dermatitis. Although sometimes contrasting, overall, they suggest that oxidative stress may have a significant role in atopic dermatitis, but our understanding is still incomplete, at least concerning in vivo data, because of limitations of available literature. Research consists of 33 papers published in 28 years, was not always performed on large study populations, represents a limited number of countries and ethnicities—not always in proportion to their size—and is scattered over multiple papers that, in the majority of cases, cannot be pooled and/or compared because many biomarkers were studied, in different tissues and with different methods. Further, larger studies appear warranted and necessary to shed more light on this aspect of atopic dermatitis, which is important not only to improve our understanding of this disease, but also for potential clinical and therapeutic implications.

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Section: Resultsmentioning

confidence: 99%

Section: Biomarkersmentioning

confidence: 96%

Oxidative Stress and Atopic Dermatitis

et al. 2020

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“…Intact skin is generally considered protective. Short-term exposure to PM 0.1 with a high content of polycyclic aromatic hydrocarbons increases 8-hydroxyl-2-deoxyguanosine, a byproduct of DNA oxidative damage, in children with eczema but not in those without eczema 28 , although particles of zinc and TiO used in topical skin care have been shown to penetrate intact skin, especially in watery or oily vehicles 29 .…”

Section: Respiratorymentioning

confidence: 99%

The health effects of ultrafine particles

2020

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Ultrafine particles (PM 0.1), which are present in the air in large numbers, pose a health risk. They generally enter the body through the lungs but translocate to essentially all organs. Compared to fine particles (PM 2.5), they cause more pulmonary inflammation and are retained longer in the lung. Their toxicity is increased with smaller size, larger surface area, adsorbed surface material, and the physical characteristics of the particles. Exposure to PM 0.1 induces cough and worsens asthma. Metal fume fever is a systemic disease of lung inflammation most likely caused by PM 0.1. The disease is manifested by systemic symptoms hours after exposure to metal fumes, usually through welding. PM 0.1 cause systemic inflammation, endothelial dysfunction, and coagulation changes that predispose individuals to ischemic cardiovascular disease and hypertension. PM 0.1 are also linked to diabetes and cancer. PM 0.1 can travel up the olfactory nerves to the brain and cause cerebral and autonomic dysfunction. Moreover, in utero exposure increases the risk of low birthweight. Although exposure is commonly attributed to traffic exhaust, monitored students in Ghana showed the highest exposures in a home near a trash burning site, in a bedroom with burning coils employed to abate mosquitos, in a home of an adult smoker, and in home kitchens during domestic cooking. The high point-source production and rapid redistribution make incidental exposure common, confound general population studies and are compounded by the lack of global standards and national reporting. The potential for PM 0.1 to cause harm to health is great, but their precise role in many illnesses is still unknown and calls for more research.

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“…This increase was associated with the level of UFP and particles' PAH content. 132 The deleterious cardiovascular effects of UFP are continuously being reported by studies involving human subjects. Exposure to UFP is found to be associated with altered heart rate, heart rate variability, changes in microvascular function, and systemic inflammation.…”

Section: The Impact Of Ambient Ufp and Np On Human Healthmentioning

confidence: 99%

A work group report on ultrafine particles (American Academy of Allergy, Asthma & Immunology): Why ambient ultrafine and engineered nanoparticles should receive special attention for possible adverse health outcomes in human subjects

Georas

Alexis

et al. 2016

Journal of Allergy and Clinical Immunology

215

136

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Ultrafine particles are airborne particulates of less than 100 nm in aerodynamic diameter. Examples of ultrafine particles are diesel exhaust particles, products of cooking, heating and wood burning in indoor environments, and more recently, products generated through the use of nanotechnology. Studies have shown that ambient ultrafine particles have detrimental effects on both the cardiovascular and respiratory systems, including a higher incidence of atherosclerosis and the exacerbation rate of asthma. Ultrafine particles have been found to alter in vitro and in vivo responses of the immune system to allergens and may also play a role in allergen sensitization. The inflammatory properties of ultrafine particles may be mediated by a number of different mechanisms, including the ability to produce reactive oxygen species, leading to the generation of pro-inflammatory cytokines and airway inflammation. In addition, because of their small size, ultrafine particles also have unique distribution characteristics in the respiratory tree and circulation and may be able to alter cellular function in ways that circumvent normal signaling pathways. Additionally, ultrafine particles can penetrate intracellularly and potentially cause DNA damage. The recent advances in nanotechnology, while opening up new opportunities for the advancement of technology and medicine, could also lead to unforeseen adverse health effects in exposed humans. Further research is needed to clarify the safety of nanoscale particles, as well as the elucidation of the possible beneficial use of these particulates to treat disease.

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Exposure to ambient ultrafine particles and urinary 8-hydroxyl-2-deoxyguanosine in children with and without eczema

Cited by 25 publications

References 45 publications

Oxidative Stress and Atopic Dermatitis

Oxidative Stress and Atopic Dermatitis

The health effects of ultrafine particles

A work group report on ultrafine particles (American Academy of Allergy, Asthma & Immunology): Why ambient ultrafine and engineered nanoparticles should receive special attention for possible adverse health outcomes in human subjects

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