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.

Metabolites of Trichoderma species isolated from damp building materials.

Buildings that have been flooded often have high concentrations of Trichoderma spores in the air while drying. Inhaled spores and spore and mycelial fragments contain large amounts of fungal glucan and natural products that contribute to the symptoms associated with indoor mould exposures. In this study, we considered both small molecules and peptaibol profiles of T. atroviride, T. koningiopsis, T. citrinoviride, and T. harzianum strains obtained from damp buildings in eastern Canada. Twenty-residue peptaibols and sorbicillin-derived metabolites (1-6) including a new structure, (R)-vertinolide (1), were characterized from T. citrinoviride. Trichoderma koningiopsis produced several koninginins (7-10), trikoningin KA V, and the 11-residue lipopeptaibols trikoningin KB I and trikoningin KB II. Trichoderma atroviride biosynthesized a mixture of 19-residue trichorzianine-like peptaibols, whereas T. harzianum produced 18-residue trichokindin-like peptaibols and the 11-residue harzianin HB I that was subsequently identified from the studied T. citrinoviride strain. Two α-pyrones, 6-pentyl-pyran-2-one (11) and an oxidized analog (12), were produced by both T. atroviride and T. harzianum. Aside from exposure to low molecular weight natural products, inhalation of Trichoderma spores and mycelial fragments may result in exposure to membrane-disrupting peptaibols. This investigation contributes to a more comprehensive understanding of the biologically active natural products produced by fungi commonly found in damp buildings.

Mold allergy: is it real and what do we do about it?

INTRODUCTION: fungi produce substances that contain pathogen-associated molecular patterns (pamps) and damage-associated molecular patterns (damps) which bind to pattern recognition receptors, stimulating innate immune responses in humans. they also produce allergens that induce production of specific ige. Areas covered: In this review we cover both innate and adaptive immune responses to fungi. Some fungal products can activate both innate and adaptive responses and in doing so, cause an intense and complex health effects. Methods of testing for fungal allergy and evidence for clinical treatment including environmental control are also discussed. In addition, we describe controversial issues including the role of Stachybotrys and mycotoxins in adverse health effects. Expert commentary: Concerns about long-term exposure to fungi have led some patients, attorneys and fungus advocates to promote fears about a condition that has been termed toxic mold syndrome. This syndrome is associated with vague symptoms and is believed to be due to exposure to mycotoxins, though this connection has not been proven. Ultimately, more precise methods are needed to measure both fungal exposure and the resulting health effects. Once that such methods become available, much of the speculation will be replaced by knowledge.