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. This article 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 their patient’s treatment plan. 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 result in 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

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

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

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

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 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 the new 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 10–64, depending on the family relationship, and were higher in brothers (64.0; p=0.04), fathers (42.9; p=0.004) and males (50.7; p<0.001) compared to sisters, mothers and females, respectively. Risk of EoE for other siblings was 2.4%. In the Nuclear-Families, combined gene and common environment heritability (h(gc)(2)) was 72.0±2.7% (p<0.001). In the Twins cohort, genetic heritability was 14.5±4.0% (p<0.001), and common family environment contributed 81.0±4% (p<0.001) to phenotypic variance. Proband-wise concordance in MZ co-twins was 57.9±9.5% compared to 36.4±9.3% in DZ (p=0.11). Greater birth-weight difference between twins (p=0.01), breastfeeding (p=0.15) and Fall birth season (p=0.02) were associated with twin discordance in disease status. CONCLUSIONS: EoE recurrence risk ratios are increased 10–64-fold compared with the general population. EoE in relatives is 1.8–2.4%, depending upon relationship and sex. Nuclear-Family heritability appeared to be high (72.0%). However, Twins cohort analysis revealed a powerful role for common environment (81.0%) compared with additive genetic heritability (14.5%)