Pollutants and asthma: role of air toxics.

Asthma is a disease characterized by intermittent bronchoconstriction due to increased airway reactivity to both allergic and nonallergic stimuli. Most asthma exacerbations that result in hospitalization are associated with viral upper respiratory tract infections. Such infections typically induce T-helper type 1 (T(H)1) responses in the airway, involving activation of nuclear factor-kappaB (NF-Kappa B). However, a more recently appreciated cause of asthma exacerbation is exposure to pollutants, including ozone and various components of particulate matter (PM), including transition metals, diesel exhaust, and biologicals such as endotoxin. Although the role of air toxics in asthma pathogenesis remains incompletely examined, many components of PM that are active exacerbants of asthma are also prominent air toxics (metal ions and organic residues). These agents have been observed to activate NF-Kappa B. Reviewed in this article are the actions of specific air pollutants on airway inflammation in humans and potential common response pathways for ozone, PM, and several air toxics

Pollutants and asthma: role of air toxics.

Asthma is a disease characterized by intermittent bronchoconstriction due to increased airway reactivity to both allergic and nonallergic stimuli. Most asthma exacerbations that result in hospitalization are associated with viral upper respiratory tract infections. Such infections typically induce T-helper type 1 (T(H)1) responses in the airway, involving activation of nuclear factor-kappaB (NF-Kappa B). However, a more recently appreciated cause of asthma exacerbation is exposure to pollutants, including ozone and various components of particulate matter (PM), including transition metals, diesel exhaust, and biologicals such as endotoxin. Although the role of air toxics in asthma pathogenesis remains incompletely examined, many components of PM that are active exacerbants of asthma are also prominent air toxics (metal ions and organic residues). These agents have been observed to activate NF-Kappa B. Reviewed in this article are the actions of specific air pollutants on airway inflammation in humans and potential common response pathways for ozone, PM, and several air toxics

Infant Drowning Prevention: Insights from a New Ecological Psychology Approach

Drowning causes significant mortality and morbidity globally, and infants (0–4 years of age) are disproportionately impacted. In a groundbreaking approach to pediatric drowning prevention, ecological psychology has been used to investigate the relationship between infants’ perceptual–motor development and their behavior around bodies of water. In this review, we summarize recent research findings in the field of ecological psychology and apply these to the prevention of infant drowning. Studies have linked infants’ avoidance of falls into the water with locomotor experience and type of accessway into bodies of water. Through crawling experience, infants learn to perceive the risk of falling into water and start adapting their behavior to avoid drop-offs leading into water. Infants tend to enter deep water more when the access is via a slope than via a drop-off. We propose that ecological psychology can enhance infant drowning prevention interventions. The aim is to create an additional layer of protection, the perceptual information layer, in addition to existing strategies, such as supervision and barriers. This new protective layer can be a powerful tool to further highlight the risk of entering the water and reduce infant drowning-related mortality and morbidity

Role of GSTM1 in resistance to lung inflammation

Lung inflammation resulting from oxidant/antioxidant imbalance is a common feature of many lung diseases. In particular, the role of enzymes regulated by the NF-E2-related factor 2 (Nrf2) transcription factor has recently received increased attention. Among these antioxidant genes, the glutathione S-transferase mu 1 (GSTM1) has been most extensively characterized since it has a null polymorphism which is highly prevalent in the population and associated with increased risk of inflammatory lung diseases. Present evidence suggests that GSTM1 acts through interactions with other genes and environmental factors, especially air pollutants. Here, we review GSTM1 gene expression and regulation and summarize the findings from epidemiological, clinical, animal and in vitro studies on the role played by GSTM1 in lung inflammation. We discuss limitations in the existing knowledge base and future perspectives and evaluate the potential of pharmacologic and genetic manipulation of the GSTM1 gene to modulate pulmonary inflammatory responses

87th Annual Georgia Public Health Association Meeting & Conference Report

The 87th Annual Meeting of the Georgia Public Health Association (GPHA) was held in Atlanta, Georgia, on March 22-23, 2016, with pre-conference (March 21st) and post-conference (March 23rd) Executive Board meetings. As Georgia’s leading forum for public health researchers, practitioners, and students, the annual meeting of the GPHA brings together participants from across the state to explore recent developments in the field and to exchange techniques, tools, and experiences. In recent years the venue for the GPHA annual conference has been Atlanta, with the 2017 GPHA Annual Meeting and Conference also scheduled to be held in Atlanta. Several new initiatives were highlighted as part of this year’s conference. These included three pre-conference workshops, expansion of academic sponsorships, an enhanced exhibit hall integrated with the poster sessions, silent auction, breaks and President’s Reception, an information booth, and an inaugural administration section track. The 2016 Annual Meeting & Conference added the Certified in Public Health (CPH) Continuing Education (CE) designation. The theme for the conference was Understanding Public Health: Research, Evidence and Practice, which reflects the science of public health

In vivo γ-tocopherol supplementation decreases systemic oxidative stress and cytokine responses of human monocytes in normal and asthmatic subjects

We have recently reported that gamma tocopherol (γT) reduces allergen and zymosan-induced inflammation using rodent models. As an initial step in extending these observations to humans, we conducted an open-label, Phase I dosing study of two doses (one or two capsules/daily for one week) of a gamma tocopherol rich preparation containing 623mg of γ tocopherol, 61.1mg of d-α-tocopherol, 11.1 mg of d-β-tocopherol (11.1mg), and 231 mg of d-σ-tocopherol per capsule. Endpoints for this study include serum levels of 5-nitro-gamma tocopherol, as a marker of oxidative stress, and changes in serum gamma, alpha and delta tocopherol and γ-2′-carboxyethyl-6-hydroxychroman (CEHC) six and 24 hours after the first dose and after 1 week of treatment. To assess biological activity of this treatment, we obtained peripheral blood mononuclear cells at baseline and after 1 week of treatment with 2 capsules of a gamma tocopherol rich preparation/day, and examined the inflammatory cytokine response of these cells in culture to ex-vivo endotoxin/LPS (0.01 ng/ml) challenge. We also monitored a number of safety endpoints to examine how well this preparation is tolerated in 8 normal volunteers (4 allergic and 4 non-allergic) and 8 allergic asthmatics. We further obtained human monocytes from a subset of these volunteers and treated them ex vivo with γT, αT,γ-CEHC and α-CEHC and assessed their actions on LPS induced degradation of IkBα, and JNK signaling and ROS generation. As detailed herein, this open label study demonstrates that gamma tocopherol enriched supplementation decreased systemic oxidative stress, increased serum levels of gamma tocopherol, and inhibited monocyte responses to LPS without any adverse health effects. Further,in vitro treatment of human monocytes with γ-CEHC and α-CEHC inhibits ROS generation and LPS-induced degradation of IκB and JNK activation

Environmental effects on immune responses in patients with atopy and asthma

Despite attempts and some successes to improve air quality over the decades, current U.S. national trends suggest that exposure to outdoor and indoor air pollution remains a significant risk factor for both the development of asthma and the triggering of asthma symptoms. Emerging science also suggests that environmental exposures during the prenatal period and early childhood years increase the risk of developing asthma. Multiple mechanisms mediate this risk as a wide range of deleterious air pollutants contribute to the pathogenesis of asthma, across a variety of complex asthma phenotypes. In this review, we will consider the role of altered innate and adaptive immune responses, gene by environment interactions, epigenetic regulation, and possibly gene by environment by epigene interactions. Gaining a greater understanding of the mechanisms that underlie the impact of exposure to air pollution on asthma, allergies, and other airway diseases can identify targets for therapy. Such interventions will include pollutant source reduction amongst those most exposed and most vulnerable, and novel pharmaceutical strategies to reduce asthma morbidity

Phase One of a Global Evaluation of Suction-Based Airway Clearance Devices in Foreign Body Airway Obstructions: A Retrospective Descriptive Analysis

Background: Choking is a prevalent source of injury and mortality worldwide. Traditional choking interventions, including abdominal thrusts and back blows, have remained the standard of care for decades despite limited published data. Suction-based airway clearance devices (ACDs) are becoming increasingly popular and there is an urgent need to evaluate their role in choking intervention. The aim of this study was to describe the effectiveness (i.e., resolution of choking symptoms) and safety (i.e., adverse events) of identified airway clearance devices interventions to date. Methods: This retrospective descriptive analysis included any individual who self-identified to manufacturers as having used an ACD as a choking intervention prior to 1 July 2021. Records were included if they contained three clinical variables (patient’s age, type of foreign body, and resolution of choking symptoms). Researchers performed data extraction using a standardized form which included patient, situational, and outcome variables. Results: The analysis included 124 non-invasive (LifeVac©) and 61 minimally invasive (Dechoker©) ACD interventions. Median patient age was 40 (LifeVac©, 2–80) and 73 (Dechoker©, 5–84) with extremes of age being most common [<5 years: LifeVac© 37.1%, Dechoker© 23.0%; 80+ years: 27.4%, 37.7%]. Food was the most frequent foreign body (LifeVac© 84.7%, Dechoker© 91.8%). Abdominal thrusts (LifeVac© 37.9%, Dechoker© 31.1%) and back blows (LifeVac© 39.5%, Dechoker© 41.0%) were often co-interventions. Resolution of choking symptoms occurred following use of the ACD in 123 (LifeVac©) and 60 (Dechoker©) cases. Three adverse events (1.6%) were reported: disconnection of bellows/mask during intervention (LifeVac©), a lip laceration (Dechoker©), and an avulsed tooth (Dechoker©). Conclusion: Initial available data has shown ACDs to be promising in the treatment of choking. However, limitations in data collection methods and quality exist. The second phase of this evaluation will be an industry independent, prospective assessment in order to improve data quality, and inform future choking intervention algorithms

Environmental determinants of allergy and asthma in early life

Allergic disease prevalence has increased significantly in recent decades. Primary prevention efforts are being guided by study of the exposome (or collective environmental exposures beginning during the prenatal period) to identify modifiable factors that affect allergic disease risk. In this review we explore the evidence supporting a relationship between key components of the external exposome in the prenatal and early-life periods and their effect on atopy development focused on microbial, allergen, and air pollution exposures. The abundance and diversity of microbial exposures during the first months and years of life have been linked with risk of allergic sensitization and disease. Indoor environmental allergen exposure during early life can also affect disease development, depending on the allergen type, dose, and timing of exposure. Recent evidence supports the role of ambient air pollution in allergic disease inception. The lack of clarity in the literature surrounding the relationship between environment and atopy reflects the complex interplay between cumulative environmental factors and genetic susceptibility, such that no one factor dictates disease development in all subjects. Understanding the effect of the summation of environmental exposures throughout a child's development is needed to identify cost-effective interventions that reduce atopy risk in children