Air pollution significantly associated with severe ocular allergic inflammatory diseases.

Ambient air pollution is a well-recognized risk for various diseases including asthma and heart diseases. However, it remains unclear whether air pollution may also be a risk of ocular allergic diseases. Using a web-based, nation-wide, cross-sectional study design, we examined whether the level of ambient air pollution is significantly associated with the prevalence of ocular allergic diseases. A web-based questionnaire was posted to invite the participants who are members of the Japan Ophthalmologist Association and their family members. The answers from 3004 respondents were used to determine whether there were significant associations between the level of the pollutants and the prevalence of ocular allergic diseases. The study period was between March to May 2017. The data of the air pollutants during 2012 to 2016 were obtained from the National Institute for Environmental Studies. The prevalence of allergic diseases was calculated by post stratification and examined for significant associations with the level of pollutants using multiple logistic regression analyses. The prevalence of seasonal allergic conjunctivitis, perennial allergic conjunctivitis, atopic keratoconjunctivitis (AKC), and vernal keratoconjunctivitis (VKC) in Japan was 45.4%, 14.0%, 5.3%, and 1.2%, respectively. The high prevalence of the severe forms of allergic conjunctivitis, including AKC and VKC, were significantly associated with the levels of the air pollutants. The prevalence of AKC was significantly associated with the levels of NO2 with an odds ratio (OR) of 1.23 (per quintile). The prevalence of VKC was significantly associated with the levels of NOx and PM10 with ORs of 1.72 and 1.54 respectively. The significant associations between the prevalence of AKC and VKC and the levels of air pollutants indicate that clinicians need to be aware that air pollutants may pose serious risks of vision threatening severe ocular allergy.

Pediatric asthma and ambient pollutant levels in industrializing nations.

Asthma is one of the most common chronic diseases in childhood and its prevalence has been increasing within industrializing nations. The contribution of ambient pollutants to asthma symptomatology has been explored in some countries through epidemiological investigations, molecular analysis and monitoring functional outcomes. The health effects of rising environmental pollution have been of increasing concern in industrializing nations with rising urbanization patterns. This review article provides an overview of the link between pediatric asthma and exposure to rising sources of urban air pollution. It primarily focuses on the asthma-specific effects of sulfur dioxide, nitrogen dioxide, ozone and particulate matter. Worldwide trends of asthma prevalence are also provided which detail the prominent rise in asthma symptoms in many urban areas of Africa, Latin America and Asia. The molecular and functional correlation of ambient pollutants with asthma-specific airway inflammation in the pediatric population are also highlighted. The final aspect of the review considers the correlation of motor vehicle, industrial and cooking energy sources, ascribed as the major emitters among the pollutants in urban settings, with asthma epidemiology in children.

Nitrogen dioxide and allergic sensitization in the 2005-2006 National Health and Nutrition Examination Survey.

BACKGROUND: Allergic sensitization is a risk factor for asthma and allergic diseases. The relationship between ambient air pollution and allergic sensitization is unclear. OBJECTIVE: To investigate the relationship between ambient air pollution and allergic sensitization in a nationally representative sample of the US population. METHODS: We linked annual average concentrations of nitrogen dioxide (NO2), particulate matter ≤10 µm (PM10), particulate matter ≤2.5 µm (PM2.5), and summer concentrations of ozone (O3), to allergen-specific immunoglobulin E (IgE) data for participants in the 2005-2006 National Health and Nutrition Examination Survey (NHANES). In addition to the monitor-based air pollution estimates, we used the Community Multiscale Air Quality (CMAQ) model to increase the representation of rural participants in our sample. Logistic regression with population-based sampling weights was used to calculate adjusted prevalence odds ratios per 10 ppb increase in O3 and NO2, per 10 µg/m(3) increase in PM10, and per 5 µg/m(3) increase in PM2.5 adjusting for race, gender, age, socioeconomic status, smoking, and urban/rural status. RESULTS: Using CMAQ data, increased levels of NO2 were associated with positive IgE to any (OR 1.15, 95% CI 1.04, 1.27), inhalant (OR 1.17, 95% CI 1.02, 1.33), and indoor (OR 1.16, 95% CI 1.03, 1.31) allergens. Higher PM2.5 levels were associated with positivity to indoor allergen-specific IgE (OR 1.24, 95% CI 1.13, 1.36). Effect estimates were similar using monitored data. CONCLUSIONS: Increased ambient NO2 was consistently associated with increased prevalence of allergic sensitization.

A review on human health perspective of air pollution with respect to allergies and asthma.

The increase in cases of asthma and allergies has become an important health issue throughout the globe. Although these ailments were not common diseases a few short decades ago, they are now affecting a large part of the population in many regions. Exposure to environmental (both outdoor and indoor) pollutants may partially account for the prevalence of such diseases. In this review, we provide a multidisciplinary review based on the most up-to-date survey of literature regarding various types of airborne pollutants and their associations with asthma-allergies. The major pollutants in this respect include both chemical (nitrogen dioxide, ozone, sulfur dioxide, particulate matter, and volatile organic compounds) and biophysical parameters (dust mites, pet allergens, and mold). The analysis was extended further to describe the development of these afflictions in the human body and the subsequent impact on health. This publication is organized to offer an overview on the current state of research regarding the significance of air pollution and its linkage with allergy and asthma.

Being overweight increases susceptibility to indoor pollutants among urban children with asthma.

BACKGROUND: Both being overweight and exposure to indoor pollutants, which have been associated with worse health of asthmatic patients, are common in urban minority populations. Whether being overweight is a risk factor for the effects of indoor pollutant exposure on asthma health is unknown. OBJECTIVES: We sought to examine the effect of weight on the relationship between indoor pollutant exposure and asthma health in urban minority children. METHODS: One hundred forty-eight children (age, 5-17 years) with persistent asthma were followed for 1 year. Asthma symptoms, health care use, lung function, pulmonary inflammation, and indoor pollutants were assessed every 3 months. Weight category was based on body mass index percentile. RESULTS: Participants were predominantly African American (91%) and had public health insurance (85%). Four percent were underweight, 52% were normal weight, 16% were overweight, and 28% were obese. Overweight or obese participants had more symptoms associated with exposure to fine particulate matter measuring less than 2.5 µm in diameter (PM2.5) than normal-weight participants across a range of asthma symptoms. Overweight or obese participants also had more asthma symptoms associated with nitrogen dioxide (NO2) exposure than normal-weight participants, although this was not observed across all types of asthma symptoms. Weight did not affect the relationship between exposure to coarse particulate matter measuring between 2.5 and 10 µm in diameter and asthma symptoms. Relationships between indoor pollutant exposure and health care use, lung function, or pulmonary inflammation did not differ by weight. CONCLUSION: Being overweight or obese can increase susceptibility to indoor PM2.5 and NO2 in urban children with asthma. Interventions aimed at weight loss might reduce asthma symptom responses to PM2.5 and NO2, and interventions aimed at reducing indoor pollutant levels might be particularly beneficial in overweight children.

Airway epithelial regulation of allergic sensitization in asthma.

While many of the contributing cell types and mediators of allergic asthma are known, less well understood are the factors that influence the development of allergic responses that lead to the development of allergic asthma. As the first airway cell type to respond to inhaled factors, the epithelium orchestrates downstream interactions between dendritic cells (DCs) and CD4⁺ T cells that quantitatively and qualitatively dictate the degree and type of the allergic asthma phenotype, making the epithelium of critical importance for the genesis of allergies that later manifest in allergic asthma. Amongst the molecular processes of critical importance in airway epithelium is the transcription factor, nuclear factor-kappaB (NF-κB). This review will focus primarily on the genesis of pulmonary allergies and the participation of airway epithelial NF-κB activation therein, using examples from our own work on nitrogen dioxide (NO2) exposure and genetic modulation of airway epithelial NF-κB activation. In addition, the mechanisms through which Serum Amyloid A (SAA), an NF-κB-regulated, epithelial-derived mediator, influences allergic sensitization and asthma severity will be presented. Knowledge of the molecular and cellular processes regulating allergic sensitization in the airways has the potential to provide powerful insight into the pathogenesis of allergy, as well as targets for the prevention and treatment of asthma.

Ozone exposure and its influence on the worsening of childhood asthma.

BACKGROUND: It is well documented that high levels of many airborne pollutants can adversely affect many systems of the human body. The aim of this study was to evaluate the specific impact of ozone (O(3)) on the worsening of childhood asthma, comparing children living at regions with high and low O(3) concentrations (reference site) without the confounding effects of other pollutants. METHODS: Pollutant concentrations were monitored and data concerning asthma prevalence were collected through a questionnaire. The studied population consisted of 478 children aged 6-13 years old enrolled in four schools of the municipalities where monitoring was performed. Remote sites were identified with very low concentrations of nitrogen dioxide and volatile organic compounds and high concentrations of O(3). RESULTS: The prevalence of wheeze for lifetime period and in the past year was 15.9% and 6.3%, respectively. Asthmatic children were identified when dyspnoea and wheezing were simultaneously mentioned in the absence of upper respiratory infections; according to that, the lifetime prevalence of asthmatic symptoms at the remote sites was 7.1%. The comparison with other previous studies was difficult because the criteria for analysis are not conveniently established. CONCLUSION: The prevalence of childhood asthmatic symptoms was about 4% higher at the high O(3) site than at the low O(3) site.

Toxicological mechanisms underlying oxidant pollutant-induced airway injury.

The health effect of atmospheric pollution is causing increasing public concern. Several controlled human-exposure studies have clearly. shown that oxidant pollutants, including ozone, nitrogen dioxide, and diesel exhaust, induce an acute inflammatory response in human airways. The main component of this response involves the influx of polymorphonuclear leukocytes (PMN) and is mediated via the upregulation of transcription factors NF-kappa B, AP-1, and NF-IL6; leukocyte-endothelial adhesion molecules, and chemokine secretion, including IL-8 and Gro-alpha. The results of recent studies also suggest that short-term exposure to ozone leads to neurogenic inflammation by causing damage to the bronchial epithelium and stimulating subepithelial sensory nerves to release substance P. In addition, such exposures lead to the consumption of endogenous antioxidants that are present in the airway lining fluid. Studies in asthmatics have shown that oxidant pollutants, including ozone and nitrogen dioxide, induce PMN influx in the airways and potentiate responses to inhaled aero-allergens. This article will review various studies addressing the toxicological mechanisms underlying oxidant pollutant-induced airways injury.

Humoral immunodepression following acute NO2 exposure in normal and adrenalectomized mice.

The effects following 20 ppm NO2 exposure on humoral immunity were investigated in C57Bl/6 mice after 48, 72, and 96 h exposure. Both spleen plaque-forming cell (PFC) responses and serum hemagglutinins (HA) using sheep red blood cells (SRBC) as antigen were studied. Splenic and thymic weight and cellularity decreased on acute exposure to NO2. PFC were markedly depressed after 48 h exposure and continued to decrease as exposure time was lengthened. HA titers were also depressed. The same significant suppression of PFC and HA titers was observed in adrenalectomized mice after 96 h NO2 exposure. The depression of humoral immunity in NO2-exposed mice was independent of stress-induced endogenous steroids.

Enhancement of antibody response in Japanese quails by acute NO2 exposure.

The effect of acute exposure to nitrogen dioxide (NO2) on anti-SRBC antibody response in two lines of Japanese quails, high and low responder, was investigated. Mean survival time of 11- to 13-week-old quails after exposure to 20 ppm NO2 was 12.0 hr. The high responder line lived longer than the low responder line. Changes of spleen weights of both lines were not observed in 10- and 20-ppm NO2 exposure for 4 hr. Anti-SRBC antibody response in high responder quail was significantly enhanced by 20-ppm NO2 exposure for 4 hr and the response in low responder quail was slightly enhanced. A similar, although somewhat less pronounced, tendency was observed also after 10-ppm NO2 exposure. These results suggest that acute NO2 exposure enhances the antibody response of Japanese quails.

Oxidant-induced enhanced sensitivity to infection in animal models and their extrapolations to man.

Animal studies have provided the toxicologist with useful and scientifically sound information indicating that exposure to oxidant gases can alter the functioning of the host's normal pulmonary defense system, resulting in an increased risk to infectious disease. Since the basic mechanisms of action of the human and the animal pulmonary defenses are similar, it is reasonable to relate these animal's biological responses to human exposures. This paper examines the possibility of quantitatively extrapolating such animal dose-response data to humans.