Presenter Bio: Claire Bird
Dr Bird is a committed and driven Scientist and business owner delivering healthier buildings through a research, commercial and academic laboratory management, training, and consulting background. Claire completed a Doctoral degree in Bioaerosol detection and characterisation in 2004 before moving to Australia to establish the Environmental Biotechnology laboratory at Flinders University. Today, she is dedicated to delivery of established and cutting-edge microbial analytical products, processes and services through her Australian based laboratory, LITMAS. Claire has operated and managed some of Australia’s largest building contamination projects, uniquely positioning her at the junction of scientific research and real-world application. Claire is involved in ongoing research and development in the area of indoor air quality and the indoor microbiome. She is participating in the Macquarie University NHMRC research project into biotoxin-related illness with scientists, engineers, patients and clinicians, as well as supporting devel0pment through newly announced Queensland University of Technology IAQ School. She is frequently asked for written and verbal presentation on the topic of indoor air quality and disease transmission. Claire loves connecting people who can support each other’s work, and strongly advocates for better Indoor Air Quality, volunteering extensively as a subject matter expert and liaison point across a speciality and geographically diverse range of indoor air quality (IAQ) associated National and International professional bodies and organisations. Former elected inaugural President of the Indoor Air Quality Association Australia and Chapter Director of the global Indoor Air Quality Association, Claire now operates as Executive Director of the global-based Integrated Biosciences and Built Environment Consortium (IBEC) who coordinates a team of world leading scientific advisers around pathogens, people, and buildings. Through this work she has been heavily involved in the roll out of the CDC-funded Commit 2 CARE program developed with the American Industrial Hygiene Association and supported by AIOH, as an easily accessible platform for self-assessment of how best to mitigate infection spread for individuals and businesses.
Research shows that measurable visible signs of dampness and musty odour strength better predict mycoaerosol-induced asthma than culture-based or culture-independent impaction sampling methods.
Airborne mold (mycoaerosol) comprises fungal particulate matter ranging in size from nanometre-sized cell fragments and extraneous DNA to spore clusters up to tens of micrometres in effective diameter.
Under diverse size distributions, individual particles display widely differing settling or terminal velocities. Recently suspended large spore aggregates more rapidly redeposit onto surfaces, travelling shorter distances than single spores of the same mold type. Small particles penetrate more deeply into the upper respiratory tract.
Increases in surface disturbance increase concentration of, and the size of mycoaerosol particles, as well as the probability of inhalation and particle capture during sampling. These factors may reduce simple spore count meaningfulness when assessing exposure risk and locating mould sources.
Microbial impactor characteristics mimic air velocity and particle behaviour in the respiratory tract. Large spore aggregates disrupt upon impaction, liberating smaller localised spore satellites, visible within microbial slit impactor traces. Light microscopy reveals sample uniformity differences in discrete, paired, chained or clumped fungal spores depending on incoming mycoaerosol particle size distribution.
Culture-based impaction generates a single colony for each culturable, intact, impacted particle regardless of the number of spores it contains, providing a direct measure of inhalation risk but leading to potential underestimation of spore dose.
Direct impaction can result in hundred-fold differences in estimated airborne mould spore concentration when spores are discrete rather than aggregated into a single clump; direct spore counting can overestimate mycoaerosol particle inhalation risk but allow spore and particle dose to be simultaneously estimated. When basing data analysis on comparing outdoor to indoor mould concentrations and profiles, a single spore aggregate in an outdoor sample can mean that an indoor dampness situation is missed, whilst an indoor aggregate could result in falsely labelling a building as contaminated.
It was therefore hypothesised that mold spore aggregation significantly reduces usefulness of airborne mold monitoring to identify source proximity and assess inhalation exposure risks.
Outdoor and indoor microscopy counts by taxon were compared based on mean and median average counts across the rows of an Air-O-Cell impactor. Comparisons between outputs from paired external samples and indoor samples were made using relative-percentage-difference in total mould concentrations. The Bray-Curtis index of similarity was employed to compare taxonomic profiles in a semi-quantitative manner between reference and test locations.
Extensive clustering of Cladosporium-like and Geotrichum-like spores was frequently observed in outdoor and indoor samples, and Aspergillus/Penicillium-like aggregated spores were observed more commonly indoors.
The presence of single large or clearly disrupted aggregates skewed spore concentrations in favor of spore types associated with aggregation rather than dampness and reduced similarity significantly.
Median concentrations and similarity indices, used extensively in air quality monitoring provide an additional tool for assessing risks to health, and detect different sources and causes of dampness-related mycoaerosols. By thinking harder about particle aggregation, and how air quality is impacted by dampness-related mould growth, we may start to close the current gap between air sampling outputs and damp buildings.