Insect Migration and Changes in Venom Allergy due to Climate Change.

Insects are highly successful animals. They have limited ability to regulate their temperature and therefore will expand range in response to warming temperatures. Climate change and associated rising global temperature is impacting the range and distribution of stinging insects. There is evidence that many species are expanding range toward the poles, primarily in response to warming. With expanded distribution of stinging insects, increased interaction with humans is anticipated with consequently increased rates of sting-related reactions and need for intervention. This article focuses on evidence that insects are expanding their range in response to warming temperature, increasing likelihood of human interaction.

Hymenoptera allergy and anaphylaxis: are warmer temperatures changing the impact?

PURPOSE OF REVIEW: Climate change has brought about many changes in our ecosystem. Prolongation of pollen seasons has been reported, related to earlier frost off in the spring and later onset of frost on in the fall. This review considers recent global evidence that stinging insects are redistributing toward the poles, thereby potentially increasing human exposure and risk of sting events. RECENT FINDINGS: With changing climate, particularly climate warming, range expansion of insects is occurring in both the Northern and Southern Hemispheres. Likewise, stinging insects, such as Hymenoptera and Lepidoptera, are also expanding range. Though there is scant data on associated increase of insect-related anaphylaxis, increased insect-human interaction is certain. SUMMARY: It is likely that climate change will continue to alter the distribution and population of Hymenoptera and other insects. As temperatures warm and regions become suitable for nesting and establishment of colonies, many insects will expand their territory. As already reported in Alaska, one would anticipate expansion of range, especially toward the poles, thereby increasing the probability of human encounters and likewise anaphylaxis.

Impact of weather and climate change with indoor and outdoor air quality in asthma: A Work Group Report of the AAAAI Environmental Exposure and Respiratory Health Committee.

Weather and climate change are constant and ever-changing processes that affect allergy and asthma. The purpose of this report is to provide information since the last climate change review with a focus on asthmatic disease. PubMed and Internet searches for topics included climate and weather change, air pollution, particulates, greenhouse gasses, traffic, insect habitat, and mitigation in addition to references contributed by the individual authors. Changes in patterns of outdoor aeroallergens caused by increasing temperatures and amounts of carbon dioxide in the atmosphere are major factors linked to increased duration of pollen seasons, increased pollen production, and possibly increased allergenicity of pollen. Indoor air pollution threats anticipated from climate changes include microbial and mold growth secondary to flooding, resulting in displacement of persons and need for respiratory protection of exposed workers. Air pollution from indoor burning of mosquito repellants is a potential anticipatory result of an increase in habitat regions. Air pollution from fossil fuel burning and traffic-related emissions can alter respiratory defense mechanisms and work synergistically with specific allergens to enhance immunogenicity to worsen asthma in susceptible subjects. Community efforts can significantly reduce air pollution, thereby reducing greenhouse gas emission and improving air quality. The allergist's approach to weather pattern changes should be integrated and anticipatory to protect at-risk patients.

Climate Change and the Impact on Respiratory and Allergic Disease: 2018.

PURPOSE OF REVIEW: The purpose of this paper is to review allergic respiratory disease related to indoor and outdoor exposures and to examine the impact of known and projected changes in climate. The global burden of disease directly attributed to climate change is very difficult to measure and becomes more challenging when the capacity of humans to adapt to these changes is taken into consideration. Allergic respiratory disease, such as asthma, is quite heterogenous, though closely associated with environmental and consequently immunologic interaction. Where is the tipping point? RECENT FINDINGS: Our climate has been measurably changing for the past 100 years. It may indeed be the most significant health threat of the twenty-first century, and consequently tackling climate change may be the greatest health opportunity. The impacts of climate change on human health are varied and coming more into focus. Direct effects, such as heatwaves, severe weather, drought, and flooding, are apparent and frequently in the news. Indirect or secondary effects, such as changes in ecosystems and the impact on health, are less obvious. It is these changes in ecosystems that may have the greatest impact on allergic and respiratory diseases. This review will explore some ways that climate change, current and predicted, influences respiratory disease. Discussion will focus on changing pollen patterns, damp buildings with increased mold exposure, air pollution, and heat stress.

Successful desensitization of a patient with aplastic anemia to antithymocyte globulin.

Antithymocyte globulin (ATG) is a polyclonal gamma immunoglobulin derived from either rabbit or equine serum that serves as therapy for aplastic anemia; however, ATG causes serum sickness in up to 70% and anaphylaxis in up to 5% of recipients. Intradermal (ID) skin testing has been the primary technique used to evaluate for a preexisting Gell and Coombs type I hypersensitivity reaction to ATG. There are no data reporting the predictive value of delayed reactions to ID testing on the risk of serum sickness. This study was designed to establish the importance of epicutaneous and ID skin testing before the administration of ATG through a case report and literature discussion. We report a patient with severe aplastic anemia that was successfully desensitized to ATG after a negative epicutaneous skin test and positive ID skin test. The patient had neither systemic nor localized reactions during the desensitization. Desensitization to ATG in patients with positive epicutaneous skin testing has been shown to be associated with serious and potentially life-threatening complications and should only be considered when the benefits outweigh the risks. Epicutaneous skin testing should be considered in conjunction with ID skin testing when screening for potential sensitivity to ATG. Because of the serious risk of anaphylaxis, desensitization should be performed in an intensive care unit setting in conjunction with a physician familiar with drug desensitization and the management of anaphylaxis.

Allergic bronchopulmonary aspergillosis.

There remains a lack of agreement on diagnostic criteria and approaches to treatment of patients with allergic bronchopulmonary aspergillosis (ABPA). The results of a survey of American Academy of Allergy, Asthma, & Immunology members regarding these 2 issues are presented and compared for concordance with published recommendations. The literature was reviewed for pertinent reports, and an electronic survey was conducted of American Academy of Allergy, Asthma, & Immunology members and fellows regarding diagnostic criteria, numbers of patients evaluated for ABPA, and treatment approaches. From 508 respondents to the survey sent to 5155 US physicians in the American Academy of Allergy, Asthma, & Immunology database of members and fellows, 245 health professionals (48%) had treated at least 1 patient with ABPA in the previous year. For the diagnosis of ABPA, there was a difference in the threshold concentration of total serum IgE because 44.9% used ≥417 kU/L, whereas 42.0% used ≥1000 kU/L. Analysis of these findings suggests that ABPA might be underdiagnosed. With regard to pharmacotherapy, oral steroids were recommended for 97.1% of patients and oral steroids plus inhaled corticosteroids plus antifungal agent were used with 41.2% of patients. The armamentarium for treatment of ABPA includes oral corticosteroids as the initial treatment with inhaled corticosteroids used for management of persistent asthma. Azoles remain adjunctive. Published experience with omalizumab has been limited.

Twin and family studies reveal strong environmental and weaker genetic cues explaining heritability of eosinophilic esophagitis.

BACKGROUND: Eosinophilic esophagitis (EoE) is a chronic antigen-driven allergic inflammatory disease, likely involving the interplay of genetic and environmental factors, yet their respective contributions to heritability are unknown. OBJECTIVE: To quantify the risk associated with genes and environment on familial clustering of EoE. METHODS: Family history was obtained from a hospital-based cohort of 914 EoE probands (n = 2192 first-degree "Nuclear-Family" relatives) and an international registry of monozygotic and dizygotic twins/triplets (n = 63 EoE "Twins" probands). Frequencies, recurrence risk ratios (RRRs), heritability, and twin concordance were estimated. Environmental exposures were preliminarily examined. RESULTS: Analysis of the Nuclear-Family-based cohort revealed that the rate of EoE, in first-degree relatives of a proband, was 1.8% (unadjusted) and 2.3% (sex-adjusted). RRRs ranged from 10 to 64, depending on the family relationship, and were higher in brothers (64.0; P = .04), fathers (42.9; P = .004), and males (50.7; P < .001) than in sisters, mothers, and females, respectively. The risk of EoE for other siblings was 2.4%. In the Nuclear-Family cohort, combined gene and common environment heritability was 72.0% ± 2.7% (P < .001). In the Twins cohort, genetic heritability was 14.5% ± 4.0% (P < .001), and common family environment contributed 81.0% ± 4% (P < .001) to phenotypic variance. Probandwise concordance in monozygotic co-twins was 57.9% ± 9.5% compared with 36.4% ± 9.3% in dizygotic co-twins (P = .11). Greater birth weight difference between twins (P = .01), breast-feeding (P = .15), and fall birth season (P = .02) were associated with twin discordance in disease status. CONCLUSIONS: EoE RRRs are increased 10- to 64-fold compared with the general population. EoE in relatives is 1.8% to 2.4%, depending on relationship and sex. Nuclear-Family heritability appeared to be high (72.0%). However, the Twins cohort analysis revealed a powerful role for common environment (81.0%) compared with additive genetic heritability (14.5%).

The biodiversity hypothesis and allergic disease: world allergy organization position statement.

Biodiversity loss and climate change secondary to human activities are now being associated with various adverse health effects. However, less attention is being paid to the effects of biodiversity loss on environmental and commensal (indigenous) microbiotas. Metagenomic and other studies of healthy and diseased individuals reveal that reduced biodiversity and alterations in the composition of the gut and skin microbiota are associated with various inflammatory conditions, including asthma, allergic and inflammatory bowel diseases (IBD), type1 diabetes, and obesity. Altered indigenous microbiota and the general microbial deprivation characterizing the lifestyle of urban people in affluent countries appear to be risk factors for immune dysregulation and impaired tolerance. The risk is further enhanced by physical inactivity and a western diet poor in fresh fruit and vegetables, which may act in synergy with dysbiosis of the gut flora. Studies of immigrants moving from non-affluent to affluent regions indicate that tolerance mechanisms can rapidly become impaired in microbe-poor environments. The data on microbial deprivation and immune dysfunction as they relate to biodiversity loss are evaluated in this Statement of World Allergy Organization (WAO). We propose that biodiversity, the variability among living organisms from all sources are closely related, at both the macro- and micro-levels. Loss of the macrodiversity is associated with shrinking of the microdiversity, which is associated with alterations of the indigenous microbiota. Data on behavioural means to induce tolerance are outlined and a proposal made for a Global Allergy Plan to prevent and reduce the global allergy burden for affected individuals and the societies in which they live.

Climate change and our environment: the effect on respiratory and allergic disease.

Climate change is a constant and ongoing process. It is postulated that human activities have reached a point at which we are producing global climate change. It provides suggestions to help the allergist/environmental physician integrate recommendations about improvements in outdoor and indoor air quality and the likely response to predicted alterations in the earth's environment into his or her patient's treatment plan. It incorporates references retrieved from Pub Med searches for topics, including:climate change, global warming, global climate change, greenhouse gasses, air pollution, particulates, black carbon, soot and sea level, as well as references contributed by the individual authors. Many changes that affect respiratory disease are anticipated.Examples of responses to climate change include energy reduction retrofits in homes that could potentially affect exposure to allergens and irritants, more hot sunny days that increase ozone-related difficulties, and rises in sea level or altered rainfall patterns that increase exposure to damp indoor environments.Climate changes can also affect ecosystems, manifested as the appearance of stinging and biting arthropods in new areas.Higher ambient carbon dioxide concentrations, warmer temperatures, and changes in floristic zones could potentially increase exposure to ragweed and other outdoor allergens,whereas green practices such as composting can increase allergen and irritant exposure. Finally, increased energy costs may resultin urban crowding and human source pollution, leading to changes in patterns of infectious respiratory illnesses. Improved governmental controls on airborne pollutants could lead to cleaner air and reduced respiratory diseases but will meet strong opposition because of their effect on business productivity. The allergy community must therefore adapt, as physician and research scientists always have, by anticipating the needs of patients and by adopting practices and research methods to meet changing environmental conditions.

Insect anaphylaxis: where are we? The stinging facts 2012.

PURPOSE OF REVIEW: Insect allergy remains an important cause of morbidity and mortality in the United States. In 2011, the third iteration of the stinging insect hypersensitivity practice parameter was published, the first being published in 1999 and the second in 2004. Since the 2004 edition, our understanding of insect hypersensitivity has continued to expand and has been incorporated into the 2011 edition. This work will review the relevant changes in the management of insect hypersensitivity occurring since 2004 and present our current understanding of the insect hypersensitivity diagnosis and management. RECENT FINDINGS: Since the 2004 commissioning by the Joint Task Force (JTF) on Practice Parameters of 'Stinging insect hypersensitivity: a practice parameter update', there have been important contributions to our understanding of insect allergy. These contributions were incorporated into the 2011 iteration. Similar efforts were made by the European Allergy Asthma and Clinical Immunology Interest Group in 2005 and most recently in 2011 by the British Society of Allergy and Clinical Immunology. SUMMARY: Our understanding of insect allergy, including the natural history, epidemiology, diagnostic testing, and risk factors, has greatly expanded. This evolution of knowledge should provide improved long-term management of stinging insect hypersensitivity. This review will focus primarily on the changes between the 2004 and 2011 stinging insect practice parameter commissioned by the JTF on Practice Parameters, but will, where appropriate, highlight the differences between working groups.

Fungi and allergic lower respiratory tract diseases.

Asthma is a common disorder that in 2009 afflicted 8.2% of adults and children, 24.6 million persons, in the United States. In patients with moderate and severe persistent asthma, there is significantly increased morbidity, use of health care support, and health care costs. Epidemiologic studies in the United States and Europe have associated mold sensitivity, particularly to Alternaria alternata and Cladosporium herbarum, with the development, persistence, and severity of asthma. In addition, sensitivity to Aspergillus fumigatus has been associated with severe persistent asthma in adults. Allergic bronchopulmonary aspergillosis (ABPA) is caused by A fumigatus and is characterized by exacerbations of asthma, recurrent transient chest radiographic infiltrates, coughing up thick mucus plugs, peripheral and pulmonary eosinophilia, and increased total serum IgE and fungus-specific IgE levels, especially during exacerbation. The airways appear to be chronically or intermittently colonized by A fumigatus in patients with ABPA. ABPA is the most common form of allergic bronchopulmonary mycosis (ABPM); other fungi, including Candida, Penicillium, and Curvularia species, are implicated. The characteristics of ABPM include severe asthma, eosinophilia, markedly increased total IgE and specific IgE levels, bronchiectasis, and mold colonization of the airways. The term severe asthma associated with fungal sensitization (SAFS) has been coined to illustrate the high rate of fungal sensitivity in patients with persistent severe asthma and improvement with antifungal treatment. The immunopathology of ABPA, ABPM, and SAFS is incompletely understood. Genetic risks identified in patients with ABPA include HLA association and certain T(H)2-prominent and cystic fibrosis variants, but these have not been studied in patients with ABPM and SAFS. Oral corticosteroid and antifungal therapies appear to be partially successful in patients with ABPA. However, the role of antifungal and immunomodulating therapies in patients with ABPA, ABPM, and SAFS requires additional larger studies.