PREPARE Abstract.
Antimicrobial resistance poses a serious challenge to health care worldwide. Attempts to control resistance by stopping antimicrobial use have met with mixed success. Failures of a critical assumption underlying such strategies – that resistant strains suffer a disadvantage in the absence of drug (the “cost of resistance”) – may be responsible for difficulties in controlling resistance by cessation of drug use. In particular, resistance mutations may be cost free, and hence persist, in some environments or on some genetic backgrounds. Furthermore, even when resistance is initially costly, compensatory evolution – the accumulation of mutations that restore fitness while maintaining resistance – may allow resistant strains to persist. Using two pathogenic bacterial species, we propose to undertake a systematic study of the costs of resistance across multiple genetic backgrounds, as well as across a variety of relevant conditions across the human-animal-environment axis. Moreover, we will determine whether resistant pathogens take the same, or different, routes to compensation in different environments. Taking advantage of evolutionary theory, we will determine the feasibility of predicting the costs of resistance in one environment using information from another environment, which would aid in predicting the persistence of resistant strains using limited information from laboratory studies. The proposed work will provide crucial information for public health policy on strategies for controlling resistance.

Ever paid attention to the black smoke rising out of the stack pipe of a transport truck? Caught that unmistakable hydrocarbon smell that goes along with it? Transportation of people and their goods is a major culprit for deteriorating the quality of our air. And it doesn’t stop there. A long list of other activities, such as heating our homes, electricity generation at power plants, agriculture, and construction of buildings and roads, contributes to ambient air pollution. Because of the wide range of activities responsible and the complex pathways between what is emitted and what we are exposed to, air pollution is a major challenge for environmental managers.

Why all the fuss over air pollution? Well, for a long time, the fields of toxicology and epidemiology have provided evidence that our health is negatively affected by air pollution. Exposure to ambient particulate matter (PM) and ozone carries risks of premature death and illness, both in the short and long-term. In Canada, evidence also exists that NO₂ is an important risk factor for death. Collectively, data from these fields are used to support environmental policies to protect public health. Policies have been developed that limit the levels of pollution in ambient air, such as the Canadian Ambient Air Quality Standards (CAAQS) for PM and ozone set by Environment Canada. Other policies that directly limit emissions at their source have also been set, such as vehicle emission standards that limit tailpipe emissions in Canada.

Imagine a world where we don’t need vehicle emission standards because cars don’t have tailpipes. Imagine a world where energy is renewable and non-polluting. Imagine a cleaner environment. It seems nearly impossible to achieve, right? Well, it may not be as far away as we think. Emissions of pollutants in North America have been on the decline over the past few decades thanks to stricter environmental policies. Take, for example, NO_x emissions [nitrogen oxide (NO) + nitrogen dioxide (NO₂)] produced in combustion of fuels, such as from power plants or motor vehicles. NO_x undergoes changes in the atmosphere before affecting the air we breathe and has the potential to form PM. NO_x is also a major contributor to NO₂ and ozone (O₃) in the air we breathe – both powerful oxidants in the human body. Since 1990, according to Environment Canada, Canada’s NO_x emissions have declined roughly 28% as a result of policies to clean exhaust from vehicles and power plants. The result has been a steady decline in ozone and NO₂ and an overall improvement in air quality.

Clearly, if exposure to air pollution affects our health, then as policies become stricter, the health of Canadians benefits. But just how much does society benefit? And how far should policies go before they are sufficient?
Last year, our research team at ĐÓ°ÉÔ­´´ University sought to answer these questions. Our findings challenged a fundamental and long-held view in environmental economics – the law of diminishing returns. According to this law, we should strive only to reduce our emissions by so much, because the benefit of further efforts to reduce emissions diminishes the more and more we reduce. At some point, our efforts to achieve better air quality no longer make sense financially: it costs more to clean the air than it benefits society. But in a study published in 2015, we instead found quite the opposite: the cleaner the air gets, the larger the benefit of reducing our emissions a little bit more. In other words, the less and less we emit, the more effective the next ton of emission control is at reducing ozone pollution. For more, see the blog on

So why do our findings differ from the conventional view? Atmospheric chemistry dictates compounding benefits for pollutants like ozone that are formed through chemical reactions rather than being emitted directly. It tells us how things move and transform in the atmosphere up to the point where we are exposed. But there is another part to this story. How does the human body respond to pollution it is exposed to? Does the body’s response argue for compounding benefits or diminishing returns?

Characterizing the dose-response curve between pollutants like PM or NO₂ and mortality gives us insight into these questions. Epidemiologists have believed for a long time that the dose-response relationship between exposure and mortality is linear. In other words, in an already pristine environment, making the air a little bit cleaner yields the same reduction in risk as if we cleaned a dirty environment by the same amount. We would get the same benefits to health regardless of how clean the air is initially, as long as we clean it by a comparable amount. But with large cohorts tracking millions of people and their health status over time, epidemiologists now have the power to better delineate the true dose-response relationship. And more and more, studies are finding that the assumed linear relationship may just not be the case. Studies in Canada, such as the Canadian Census, Environment, and Health Cohort (CanCHEC) study have instead found non-linear dose-response relationships for the pollutants NO₂ and PM and mortality. This alternative form of dose-response curve implies that people become more sensitive to pollution as the air becomes cleaner. Or alternatively, if we continue cleaning the atmosphere by progressively reducing our emissions, we get larger and larger reductions in health risks for each small improvement in air quality. The next unit of improved air quality yields more benefit than the previous unit. Sound familiar?

In a newer research project, we worked collaboratively with experts at Health Canada to examine the policy implications of this newer, non-linear form of dose-response relationship. We linked data from CanCHEC with engineered models that track the movement and transformation of air pollutants in the atmosphere from the time they are emitted. The result? A comprehensive set of information that gives insight into how the health of Canadians is directly affected by pollution emitted at its source, whether from the tailpipe of a car or the stack of a power plant.

Our findings indicate that reducing emissions of NO_x brings health benefits of up to $1,400,000 per ton of emission. Where does this benefit come from? When we reduce NO_x, NO₂ in ambient air immediately decreases, and NO₂ is linked to death. But this is just part of the story. With the new, non-linear dose-response model found in CanCHEC, the benefits of reducing emissions increase dramatically as policies become more stringent. With Canada-wide reductions in emissions from all sources, the benefits of reducing each additional ton of emission can grow by 3 or more times. And the benefits are, more often than not, larger than what we would have predicted based on the traditional, linear dose-response curve.

In light of these increasing benefits, we might wonder how much it actually costs to reduce emissions. We have to change our technologies, and even our behaviours, to bring about these changes. So what is the price tag? Well, the answer may not be straightforward. Such costs vary with the type of source (such as vehicles and power plants), and even more so from one place to another. But, on average, the cost of reducing 1 ton of NO_x from industrial stacks can be anywhere from a few hundred dollars to a few thousand. And the costs of reducing the next ton will rise nonlinearly with stricter and stricter policies.

So, is it worth paying? Even without precise estimates of these costs, benefits clearly outweigh the costs by at least an order of magnitude. And even if costs rise as we move towards a cleaner environment, so do the benefits. It’s a race between benefits and costs and the point at which one catches the other may be much farther away than we thought previously.

The intersection of atmospheric science, epidemiology, and economics is a rapidly advancing niche of research. And one thing is clear: whether you approach this problem from an atmospheric science angle or an epidemiology one, we are finding that we ought to be doing more to emit less. Our policies ought to be stricter. We ought to take better control of our environment and our health.

Key references:

Pappin AJ, Mesbah SM, Hakami A, Schott S. 2015. Diminishing returns or compounding benefits of air pollution control? The case of NO_x and ozone. Environ Sci Technol. 49(16):9548-9556.

Pappin AJ, Hakami A, Blagden P, Nasari M, Szyszkowicz M, Burnett RT. The impact of a nonlinear concentration-response function in estimating the benefits of emissions abatement. Environ Res Lett. Under review.

By Marie-Claire Flores Pajot, Dept. of Health Sciences, ĐÓ°ÉÔ­´´ University

No child should be left out from going to school for the very first time, playing at recess with new friends, or having the opportunity to learn about what the world will offer them in life. And no family should lose these or other precious moments with their children. Unfortunately, this is the case for some. Planning visits to the oncologist as opposed to birthday parties; cheering as they see their brave children succeed a battle through chemotherapy as opposed to cheering for scoring a goal in a soccer game.

Estimates from the Canadian Cancer Society in 2014 indicate that in the next few years approximately 1450 new cases of cancer will occur annually in Canadian children under the age of 19. Thankfully, many childhood cancers can now be treated and even cured. However, treatment does not remediate the significant psychosocial and financial burden to patients and families; not to mention the dreadful journey through chemotherapy: pain, emotional distress and sleepless nights for both the young patient, and their families.

It is often forgotten that overcoming treatment is not crossing the finish line; unfortunately, quite often the battle continues. Late-effects are common and can accompany survivors for months or even decades after their cancer treatment has ended. Some of the late-effects can be emotional complications, such as anxiety and depression; other late-effects are reproductive or sexual development problems, that can affect both boys and girls well into adulthood; learning and memory difficulties are also common; and there are many physical complications such as heart problems caused by the use of anthracycline drugs during treatment, hearing problems due to radiation therapy, as well as muscle and nerve damage that can result in pain or weakness (National Cancer Institute, 2015).

New advances are aiming for early diagnosis to improve patient outcomes (Weller et al., 2012). The causes of the different cancers are complex and elusive but continue to be investigated in clinical settings, laboratories and epidemiological studies (Danaei et al., 2005). Nonetheless, there is likely a combination of genetics, lifestyle, environment and random error in cell replication and control, which influence an individual’s cancer risk (Buka, Koranteng, & Vargas, 2007; Stiller, 2004). In order to implement cancer prevention initiatives, it is important to better understand how many of the new cancer cases in a population are due to modifiable risk factors that could be prevented.

The role of the environment
The importance of our environment has been recognized to play an important role in our physical and mental health (Evans, 2003; McMorris, Villeneuve, Su, & Jerrett, 2015). Yet, we often forget that even the filtered water used for the morning coffee or tea, the background noise, the air conditioning at the office, all impacts our overall wellbeing to some degree. The significant implication of our environment shaping our health has motivated researchers to investigate possible causes to cancer at different spatial scales, from the particles that linger in our bedroom (Zhang & Smith, 2003), to the neighbourhood we live in (Eschbach, Mahnken, & Goodwin, 2005).

Environmentally derived chemicals entering the human body via food, drink or air that have been shown to, or suspected to, increase risk of developing cancer are called ‘environmental carcinogens’ (Hemminki, 1990). To date, some of the well-studied environmental carcinogens include electromagnetic fields, pesticides, and air pollution (Cancer; Zahm & Devesa, 1995). Canadian studies that have looked at recognized carcinogens emitted to the environment, found that the amounts varied considerably by province. Interestingly, the rate of new adult cancer cases is also observed to vary by province, with a declining rates moving across Canada from east to west, with the highest incidence rates in Quebec and the Atlantic provinces and the lowest rates in Alberta and BC (Canadian Cancer Society’s Advisory Committee on Cancer Statistics, 2015). These differences in incidence rates of cancer by geographic location can be driven by multiple factors, most notably differences in the age demographic of those who live in different locations. However, neither demographic differences nor lifestyle-related factors, like smoking, can fully explain these geographic variations. Exposure to environmental carcinogens has been recognized to have a significant impact on new cancer rates, and due to the observed patterns of variability of exposure across the nation, studying the extent to which these patterns co-occur with childhood cancer rates may give insight into the etiology of some cancers.

These questions have motivated researchers Drs. Alvaro Osornio-Vargas, Osmar Zaiane, David Eisenstat from the University of Alberta, and Paul Villeneuve from ĐÓ°ÉÔ­´´ University, to take a further step and investigate the associations between exposure to environmental carcinogens and the incidence of childhood cancer in Canada. This study is being funded by the  and . Using a special technique called data mining, they will study the national patterns and trends of childhood cancer and assess the relationship with multiple chemicals. Nineteen known carcinogens and 51 potential carcinogens emitted into the air by industries between 2001 and 2011 will be studied to better understand their association with cancer in children under the age of 19 years. The International Agency for Research on Cancer (IARC) classifies outdoor air pollution as a carcinogen (Simon, 2013). In urban areas, traffic is often the main source of ambient air pollution and there are increasing reports of the risks associated with proximity to high-density traffic, including risk of childhood leukemia (Raaschou-Nielsen, Hertel, Thomsen, & Olsen, 2001). Therefore, in addition to industrial emissions, this project will also examine impacts of meteorological conditions that play a role in dispersing emissions, as well as the impact of proximity to major roads.

Overall, this study hopes to improve our understanding of the extent to which the geographic variability of childhood cancer rates in Canada is associated with industrial and traffic-related pollution. The knowledge gained might support future prevention strategies for specific types of cancer. More epidemiological studies, such as this one, in conjunction with clinical studies, will identify areas where action can be taken to prevent childhood cancer, and perhaps one day children will not have to choose between which toy to bring to chemo, but instead which park to play in next.

References
Buka, I., Koranteng, S., & Vargas, A. R. O. (2007). Trends in childhood cancer incidence: review of environmental linkages. Pediatric Clinics of North America, 54(1), 177-203.

Canadian Cancer Society’s Advisory Committee on Cancer Statistics. (2015). Canadian Cancer Statistics 2015. Canadian Cancer Society.

Cancer, I. A. f. R. o. Overall Evaluations of Carcinogenicity to Humans. List of all agents, mixtures and exposures evaluated to date.

Danaei, G., Vander Hoorn, S., Lopez, A. D., Murray, C. J., Ezzati, M., & group, C. R. A. c. (2005). Causes of cancer in the world: comparative risk assessment of nine behavioural and environmental risk factors. The Lancet, 366(9499), 1784-1793.

Eschbach, K., Mahnken, J. D., & Goodwin, J. S. (2005). Neighborhood composition and incidence of cancer among Hispanics in the United States. Cancer, 103(5), 1036-1044.

Evans, G. W. (2003). The built environment and mental health. Journal of Urban Health, 80(4), 536-555.

Hemminki, K. (1990). Environmental carcinogens Chemical Carcinogenesis and Mutagenesis I (pp. 33-61): Springer.

McMorris, O., Villeneuve, P. J., Su, J., & Jerrett, M. (2015). Urban greenness and physical activity in a national survey of Canadians. Environmental research, 137, 94-100.

National Cancer Institute. (2015). Late Effects of Treatment for Childhood Cancer. Childhood Cancers.

Raaschou-Nielsen, O., Hertel, O., Thomsen, B. L., & Olsen, J. H. (2001). Air pollution from traffic at the residence of children with cancer. American journal of epidemiology, 153(5), 433-443.

Simon, S. (2013). World Health Organization: Outdoor Air Pollution Causes Cancer. American Cancer Society.

Stiller, C. A. (2004). Epidemiology and genetics of childhood cancer. Oncogene, 23(38), 6429-6444.

Weller, D., Vedsted, P., Rubin, G., Walter, F., Emery, J., Scott, S., . . . Olesen, F. (2012). The Aarhus statement: improving design and reporting of studies on early cancer diagnosis. British Journal of Cancer, 106(7), 1262-1267.

Zahm, S. H., & Devesa, S. S. (1995). Childhood cancer: overview of incidence trends and environmental carcinogens. Environmental health perspectives, 103(Suppl 6), 177.

Zhang, J. J., & Smith, K. R. (2003). Indoor air pollution: a global health concern. British medical bulletin, 68(1), 209-225.

By Colin A. Capaldi, Department of Psychology, ĐÓ°ÉÔ­´´ University

From declining biodiversity to rising sea levels, we are inundated with seemingly endless news about the deteriorating health of our planet. Terms like ecoanxiety and ecoparalysis have emerged into the lexicon to capture the sense of dread and powerlessness that might be experienced in the face of these unprecedented problems. Of course, not everyone is as concerned about environmental issues like climate change as others might be. But for the nature lovers among us, there are many reasons to be discouraged, worried, and upset.

Recent research from the offers hope for those who would rather listen to the melodies of birds instead of scrolling through tweets; gaze upon the star-filled sky instead of staring at a laptop screen in Starbucks; or smell the blossoming spring flowers instead of synthetic perfumes. Collating results from dozens of studies with over 8,000 individuals in total, we found that people who feel more subjectively connected to nature tend to be happier; they report greater satisfaction with life, more positive emotions, and a greater sense of vitality on average. Far from insignificant, these results suggest that a person’s connection to the natural world is as important of a predictor of happiness as one’s education, marital status, or physical attractiveness.

Why are the nature connected happier? One potential answer is that they spend more time in nature. A substantial body of research shows that spending even brief amounts of time in natural environments can boost emotional well-being. For instance, a previous study conducted by ĐÓ°ÉÔ­´´ professor (and my PhD supervisor) Dr. John Zelenski and CUHL alumna Dr. Lisa Nisbet found that students who were randomly assigned to take a brief walk outdoors in nature reported more positive emotions than students assigned to walk indoors through the campus tunnel system. Nature lovers may be happier because they reap the benefits of being in nature more often than those who are not as connected to the natural world.

Although people’s connection to nature tends to be fairly stable over time, it can change in the moment and be strengthened via increased nature contact. Thus, the implications are fairly obvious. Whether it is finding a few minutes each day to go outside, to bringing elements of nature indoors (e.g., adding plants to your home), connecting with the natural world is a relatively easy, cheap, and effective way to boost well-being. A growing body of research is also highlighting the benefits of having green space near one’s home. With more and more Canadians living in urban areas, it is important that enclaves of nearby nature are available to city residents for them to take advantage of.

Beyond individual well-being, these findings also have important implications for the well-being of the environment as those who feel more connected to nature are, unsurprisingly, more likely to value and want to protect it. Instead of it being a zero-sum game where our happiness has to come at the expense of the environment, we are increasingly learning that the well-being of each is inherently dependent on the other.

Based on:

Capaldi, C. A., Dopko, R. L., & Zelenski, J. M. (2014). The relationship between nature connectedness and happiness: A meta-analysis. Frontiers in Psychology, 5, 976.

Nisbet, E. K., & Zelenski, J. M. (2011). Underestimating nearby nature: Affective forecasting errors obscure the happy path to sustainability. Psychological Science, 22, 1101-1106.

An eider nest is surveyed near Cape Dorset by a team of hunters and researchers from Environment Canada and ĐÓ°ÉÔ­´´ University studying the effects of disease and predation on nesting birds.

By Jennifer Provencher, Department of Biology, ĐÓ°ÉÔ­´´ University

A striking step forward in environmental protection policy was the creation of the Minamata Convention signed by 128 countries in 2013. As of April 2015, ten countries had ratified the convention. The Convention aims to limit the release of mercury into the environment. Although mercury is naturally found in the environment, it is also released by a number of industrial processes. Methyl mercury is a known neurotoxin that affects animal development and reproduction. The most extreme example of mercury poisoning for humans is from Minamata, Japan (where the convention’s name comes from). The people of Minamata were exposed to mercury through industrial wastewater from a nearby chemical factory in the mid-1950s. The mercury released into the sea bioaccumulated in the shellfish and fish in the area, which were main food staples for the local residents. Feeding on this seafood resulted in acute mercury poisoning, causing a severe neurological disorder among humans now known as Minamata disease.

Although the Minamata Convention is potentially a huge win for environmental protection, there is much work to be done. First, there is the task of ratification by each participating country, which must alter their national legislations to align with the Minamata Convention. Once all the new legislation is in place, countries must then have programs and enforcement in place to ensure that stakeholders are compliant with the policies on release and disposal of mercury. And there is still the task of designing and implementing monitoring programs to evaluate whether the steps put into place are in fact having the desired effect of reducing mercury in the environment and in wildlife. One stage for this environmental play is the Canadian Arctic.

In the Canadian Arctic, mercury in many habitats and species has been studied, with samples from water and plankton through intermediates in the food chain up to polar bears and humans. Some of the most extensive data sets on mercury are available for animals in the Canadian Arctic, which allows researchers to study how mercury is changing in the environment over time. Seabirds have been particularly useful as study species for researchers who are interested in the effects of mercury, and the overall trends of mercury in northern ecosystems. Environment Canada researchers and its National Wildlife Specimen Bank, located on ĐÓ°ÉÔ­´´ University’s campus, have played an important supporting role in this research. Several marine birds have shown that mercury levels in the Canadian Arctic have increased since the 1970s, and continue to rise in some areas (^{Riget et al.; Science of the Total Environment doi:10.1016/j.scitotenv.2011.05.002}). A recent study looking at specimens dating back to the 1800s show that some bird species that are high in the Arctic food chain are experiencing a 45 fold increase in mercury over the last century (^{Bond et al. 2015; The Royal Society 10.1098/rspb.2015.0032}). This increase contrasts with decreases seen in persistent organic pollutants in seabird tissues following policy measures over a much shorter time frame: from the 1970s to present (^{Braune et al. 2010; Interdisciplinary Studies in Environmental Chemistry}).

Hunters return to home with eider ducks after a day of spring hunting. Samples are taken from the birds to study parasites and contaminants, and then the Hunter and Trapper Association distributes the meat among the community.

Studying and measuring mercury in marine birds each year socio-cultural perspectives. Marine birds are an integral part of both traditional culture and modern practices in northern Canada. Their eggs are collected for food during the breeding season and duck and goose down is a valuable insulating material that continues to be collected today by many for both personal use and commercial sales. Marine birds are also hunted for their meat, and their skins are used for household items such as slippers, bowls and jackets. Currently, there are many concerns in the north including rising food costs, sustainability, healthy food choices, and the need to better integrate traditional knowledge with science for ensuring viability of harvested populations. It is hard to argue with the value of marine birds as traditional foods: they are after all free range, organic, sustainable, locally grown, locally harvested, healthy to eat and grounded in cultural practices. Marine birds continue to have very low levels of mercury making birds like geese and ducks (along with caribou and other country foods) great sources of healthy, local nutrition. It is perhaps not happenstance that they are also used as ‘sample sentinels’ for studies on possible changes in pollutant levels of importance to human health.

An eider skin basket made by the Fur Production and Design class at the Nunavut Arctic College in Iqaluit as part of their annual wildlife workshop.

There are other reasons why we should be ‘keeping an eye’ on mercury in Arctic marine birds. The story of mercury cycling in the environment is much more complex than can be captured by a single international agreement. Mercury levels in northern Canada are not influenced by North American emissions, but have the potential to be greatly influenced by those from Asia. Even with the Minamata Convention in place, emissions from some regions in Asia are not predicted to slow for decades, and even when they do, it may take decades to cease increasing levels in Arctic ecosystems (^{Provencher et al. 2014; Environmental Reviews dx.doi.org/10.1139/er-2013-0072}). One only has to go to smog-filled streets of Beijing to see how distant the Canadian Arctic is. Additionally, warming trends in the north that are causing the melting of glaciers and permafrost may be releasing large quantities of mercury into the environment. The low productivity of the Arctic may also make top-level predators susceptible to bioaccumulating more mercury than their counterparts in ecosystems with higher productivity . Thus, arctic marine birds in Canada may be particularly at risk from increasing Hg levels associated with long-term Hg deposition patterns and changing climatic conditions.

Schematic of how a system with low productivity with slow growing biota may lead to exacerbated mercury burdens in top predatorsas compared with more productive, faster growing systems

Canada still needs to ratify the Minamata Convention and research is needed to continue to monitor mercury in marine birds and northern ecosystems. Through these studies, we can help determine if any policies put in place are leading to the desired outcomes (a reduction in environmental mercury). These studies also will help us understand both the acute and sub-lethal effects of mercury on organisms. This research can continue to contribute to other conversations around human health and sustainability in the Arctic, and be used to engage northern students in science, building capacity and helping people make informed decisions (^{Provencher et al. 2013; Arctic}). So although legislators have succeeded with an international agreement on mercury, it is the continued work on mercury and marine birds that has the potential to help inform and evaluate policies and also to shape education, health and culture.

Based on Provencher, J.F., Mallory, M.L., Braune, B.M., Forbes, M.R., Gilchrist, H.G., 2014. Mercury and marine birds in Arctic Canada: effects, current trends and why we should be paying closer attention. Environmental Reviews 22, 244-255.

by David McMullin, Department of Chemistry, ĐÓ°ÉÔ­´´ University

One of the most fascinating aspects of fungi is their ability to synthesize an array of structurally diverse, often potently bio-active compounds known as secondary metabolites. This phenomenon can be exemplified by Sir Alexander Fleming’s discovery of penicillin from an indoor Penicillium species, or our exploitation of these chemicals as pharmaceuticals including the cholesterol lowering statins. There is a growing body of evidence from large population studies that demonstrates individuals living or working in damp and mouldy buildings are at an increased risk of developing allergies and respiratory symptoms, including asthma.

Modern buildings are designed to be more energy efficient with lower ventilation rates compared to the buildings constructed 40 years ago. Many of the commonly used building materials today, including particle board and paper-faced gypsum wallboard, will become water saturated with much less water as opposed to wood and traditional plaster. This unwanted water indoors can originate from daily routine activities such as cooking and showering, undetected leaks or flooding. When the amount of water vapor in a building exceeds the buildings ability to remove it, it is absorbed by the building materials. When these building materials become damp, mould growth occurs. This is of particular importance to individuals from industrialized countries, including Canada, as we spend the majority of our time indoors

The specific fungi, or moulds that are found on damp building materials is related to ‘how damp”, the amount of time they remain damp and “nutrients” of the particular building material. As different commonly used building materials have their own unique combination of available water, nutrients and chemistry, it is not surprising that specific moulds are associated with certain materials. While the overall species diversity of fungi is considered great, the number of species found indoors is fairly small. Interestingly, as similar building materials are used in industrialized countries, the distributions of some of the more common moulds in temperate environments are also very similar.

Gypsum board is often used to construct interior walls and ceilings; however, when it becomes damp it promotes the growth of numerous moulds. The most commonly identified indoor mould, Penicillium rubens, is illustrated and is the species where the antibiotic penicillin was originally discovered from.

Since the changes in construction practices for buildings and homes in the 1970’s, evidence from large epidemiological studies conducted in multiple countries has shown that indoor exposures to dampness and moulds are associated with an increased risk for respiratory symptoms, asthma, bronchitis, respiratory infections and other non-specific symptoms. For example, the inflammatory disease asthma is commonly associated with a genetic predisposition known as atopy. However, individuals working or inhabiting a damp, mouldy building are at an increased risk for developing asthma. As a genetic predisposition and an allergy cannot explain this disease pattern, it suggests that there is a toxic effect. The production of toxic fungal secondary metabolites may explain why individuals are developing (non-atopic) asthma and other respiratory symptoms. As many of these secondary metabolites are not volatile, it additionally indicates that the exposures we experience are due to the inhalation of mould spores and mycelial fragments which harbor these biologically active chemicals.

To ask the question, “how do toxic secondary metabolites produced by moulds alter human lung biology?”, information on the identity of the moulds found indoors and the preparation of the toxic chemicals they produce are first required. During my graduate studies in Professor David Miller´s group, mould samples were collected from across Canada representing some of the most commonly identified fungi indoors. The goal of my research project was to purify the dominant secondary metabolites produced by these moulds so they could be tested for biological activity in relevant toxicological experiments. This type of work is necessary as one cannot typically go to the store and purchase these chemicals, you have to isolate them from nature yourself. The unambiguous confirmation of specific secondary metabolites from a particular species can often help fungal taxonomists, as the production of these chemicals is typically consistent within a particular species.

What I found investigating the secondary metabolites produced by some of the most frequently identified fungi in damp buildings ranged from the confirmation of potently toxic compounds known to be produced by certain species to the identification of new-to-science chemicals. Growing liters upon liters of fungi in liquid can be messy, stinky work…but it is a lot of fun. So, after extracting all of those liters of fungal culture, isolating the secondary metabolites and identifying the structures by various spectroscopic methods; I was left with a collection of fungal metabolites produced by the actual moulds found growing in Canadian buildings and homes.

Chemical diversity of the secondary metabolites produced by moulds found in damp buildings. Many of these toxic compounds have been studied for their inflammatory properties in relevant toxicological experiments.

A broad consensus has been reached by national (e.g., Health Canada) and international (e.g., World Health Organization) agencies on the impact of mould and dampness in buildings. With these pure metabolites, we can contribute to an understanding of the role they play in the documented health effects of those working or living in damp and mouldy buildings. At the very low exposures that could be experienced by the human lung indoors, induction of pro-inflammatory genes, acute inflammation and histopathological disruptions have been observed in relevant models by fungal metabolites, including many of the metabolites isolated during my graduate research. While there are some differences between various models, all results indicate that the compounds present on mould spores that we are exposed to in damp buildings are potently pro-inflammatory. The physiological mechanism of inflammation and immuno-modulatory effects caused by these fungal metabolites are still poorly understood in lung cells. These types of experiments have revealed that these toxins modulate genes involved in asthma at concentrations experienced in damp and mouldy buildings by the human lung. A concerted effort on this important human health research will contribute to a more comprehensive understanding for non-atopic asthma and other documented adverse health effects associated with indoor mould exposures in humans.

For more information, please see:

Miller JD and McMullin DR (2014) Fungal secondary metabolites as harmful indoor air contaminants: 10 years on. Applied Microbiology and Biotechnology, 98: 9953-9966.

Top image courtesy of Kookkai_nak at FreeDigitalPhotos.net