The use of diesel engines is increasing because they are more fuel-efficient than gasoline engines, however, diesel engines produce different emissions than gasoline engines. Diesel exhaust is emitted from the tailpipe of both “on- road” diesel engine vehicles (diesel cars, buses and trucks) and “non-road” diesel engines (locomotives, marine vessels and some construction equipment). Diesel exhaust consists of both gaseous and particulate air pollutants. Since people with asthma and allergic diseases appear to be sensitive to air pollution, we wanted to know how diesel exhaust (DE) affected their respiratory and immune systems. Below we present our research findings in this study.

Air pollution collectively describes the presence of a complex mixture of particulate matter (PM), organic compounds (e.g. polycyclic aromatic hydrocarbons and endotoxins), gases (e.g. carbon monoxide, sulfur oxides, ground-level ozone, nitrogen oxides) and metals present in indoor and outdoor air, which can cause harm or discomfort to humans or other living organisms. Although the effects of prolonged exposure to traffic-related air pollution (TrAP), specifically, are well characterized with respect to respiratory and cardiovascular outcomes, comparatively little is known about the impact of particulate matter on affective and cognitive processes, neurodegenerative effects and microcirculation. Research using animal models, along with epidemiology, has greatly enhanced our understanding of DE-related cognitive and learning outcomes, and has implicated several important potential mechanisms. However, such models are inherently limited given interspecies differences (animal models), some degree of unavoidable residual confounding (epidemiology), and a bias towards subacute or chronic effects (epidemiology). By largely overcoming these limitations, our in vivo human model, using freshly-generated exhaust that is diluted and aged to reflect real-world conditions, allows us to augment existing knowledge in a manner applicable both to current research on environmental effects on cognition, as well as current public health concerns of great relevance to Canadians. This study has finished participant enrolment and data analysis is now underway.

The detrimental effects of air pollution on cardiovascular and respiratory health are described in a large body of scientific literature. Olympic Games in cities known for high levels of air pollution such as Beijing 2008 and Athens 2000 raised concerns regarding athlete’s health and athletic performance. Ironically, especially athletes, who tend to follow a health-conscious lifestyle, are at risk of cardiorespiratory symptoms and illnesses triggered by air pollution. Physical activity leads to the release of epinephrine. Epinephrine induces a widening of the airways to facilitate the increased minute ventilations required to sustain the physical demands placed by the training loads. The inhalation of increased volumes of polluted air through widened airways, ultimately leads to an impairment in healthy lung function and athletic performance. function and athletic performance.The acute treatment of choice for these asthma-like symptoms is the inhalation of beta-2-agonists (IBA), which mimic epinephrine. While IBAs induce a further widening of the airways and relieve respiratory distress in the short-term, IBA use may increase the chance of pollutants reaching deeper areas in the bronchial tree, where they can cause structural (airway remodeling) and functional (decreased abilities to generate air flow) damage in the long term. The purpose of this proposed study is to investigate short- and long-term effects of IBA-use in the treatment of respiratory symptoms triggered by air pollution exposure in elite athletes.

Asthma is a disease associated with considerable health consequences whose prevalence has increased sharply over the past 40 years on a global level. Asthma is characterized by chronic inflammation and airway hyper-responsiveness to both irritant and allergenic exposures. While viral and allergenic exposures have been the primary focus of research of asthma exacerbation, the evidence linking combustion-derived particulate matter (PM) to asthma symptoms and exacerbations is considerable. Diesel exhaust (DE) is a key source of ambient PM less than 2.5 microns in diameter (PM2.5), which penetrates deeply into the lung and has been strongly associated with acute worsening of asthmatic lung function. Air pollution is a multi-inhalant mixture, but related research typically focuses on single exposures in each experiment. While binary “stimulus-response” types of questions are important initial steps to elucidating the mechanisms of asthma, our goal is to mimic the real-world milieu of inhaled toxicants by combining an allergen challenge with DE exposure. Therefore, our goal is to document, in humans and in-vivo, DE’s ability to augment allergen-induced immune responses (eg: oxidative stress, eosinophilia, IgE and Th2 cytokines in the lung).

Phthalates are found in high concentrations as softeners in PVC as well as in other plastics and a range of consumer products. They leak into the environment, and are ubiquitous environmental contaminants found in air, dust and food. Exposure of the general population is confirmed by the presence of phthalate metabolites in nearly all analysed urine samples. Consumer products, food and indoor environment are the main sources of phthalates, with inhalation, ingestion, dermal and mucous contact as the major exposure routes. Epidemiological studies suggest that phthalate exposure is associated with worsening or development of airway diseases, and both phthalate levels in house dust and urinary levels ofphthalates have been associated with various respiratory outcomes. This study will be the first to investigate airway effects due to inhalation of a known concentration of a single phthalate. We have chosen DBP as a model phthalate since some of the highest indoor air levels have been reported for this phthalate, and it appears to have a higher inflammatory potential in comparison to other phthalates in vitro. Allergen-sensitized (atopic) asthmatics and non-asthmatic individuals will be recruited, since the previous studies showed stronger effects in susceptible individuals.

COPD is a disease characterized by increasing airflow obstruction caused by chronic inflammation in the lung. Although smoking remains an important risk factor for COPD, accumulating evidence has identified nonsmoking risk factors that also contribute to COPD development and progression. Therefore, the rationale of this study is to further investigate the proposal that a component of ambient air pollution such as Diesel Exhaust (DE), is one such risk factor for COPD. The acute effects of DE will be examined in a cohort of patients that currently have or are at risk of developing COPD, as well as in healthy controls. The purpose of the COPA study is to provide biological plausibility and deepen mechanistic understanding of the emerging epidemiology suggesting a strong role for air pollution in COPD. The novelty of COPA is that those with COPD have never before been a specific focus of a controlled human exposure to particulate air pollution and COPA also enjoys the advantage of including healthy and at risk participants so that we may understand the very early stages of COPD development, oriented toward a framework of protection and prevention.

Chronic exposure to diesel exhaust (DE) is associated with a wide range of adverse health outcomes: e.g. cognitive impairment, vascular diseases, and increased morbidity and mortality associated respiratory illness, and DE has been classified as carcinogenic to humans (Group 1) by the International Agency for Research on Cancer (IARC). Both chronic and acute exposures to DE have been associated with respiratory illnesses; chronic DE exposure is associated with lung fibrosis and acute exposure to DE is associated with increased asthma exacerbations reflected in reduced lung function, and increased wheezing. Prominent pathophysiological and molecular mechanisms linking DE exposure to negative health outcomes include increased inflammation, oxidative stress and airway resistance. However, these molecular signatures are not specific to DE exposure, have poorly- defined dose-response relationships, and are derived from body fluids and tests that are inconvenient, expensive, and time-consuming to access and analyze. Therefore, the broad goal of this project is to elucidate a more robust signature of exposure to DE that can offer both mechanistic insight as well as temporal and, importantly, dose-response resolution. Such signature specificity and resolution will be crucial in informing both provincial and national policy and decision-makers as they work towards reasonable limits to occupational DE exposure and devise practical monitoring program.

Around 40% of the world’s population is impacted by some form of allergic disease (ie: seasonal allergies), and this number continues to rise. An allergic response is known to be caused by both genetic and environmental factors. When our bodies come in contact with allergens such as dust mites, pollen, and air pollutants (diesel exhaust particulates), this can cause changes to our genes.

Genes are made of a molecule called deoxyribonucleic acid, or DNA for short. There is also another type of molecule called ribonucleic acid (RNA) that works closely with your genes. All of this is contained inside cells within your body. Changes to the genes or RNA may affect a person’s chance of developing certain diseases. Changes can be inherited (passed on in families from parents to children) or caused by external factors such as allergen or pollution exposures described above. Changes can be permanent or they can come and go. When genes are affected by the environment, we call it an epigenetic modification.

This study is trying to identify the epigenetic modifications that happen when the human body is exposed to allergens and pollution, something that we encounter on a daily basis. To take that question further, we also want to know if Budesonide (Rhinocort®), a nasal spray corticosteroid medication that is often used to treat allergen responses, can reverse the epigenetic modifications caused by the exposures. Being able to understand what changes occur with or without the drug under the different exposure will help researchers optimize more effective treatments for future use.

The bugs in our nose and lungs (airway microbes) include those that are pathogenic (cause disease) and those that are simply colonizing (living in airways but not causing disease). By definition, the bugs living in our airways originated elsewhere, and that source may well be the air in our primary living space (our homes). We propose to test this idea by testing the air in home environments of those with common airway diseases (like chronic obstructive pulmonary disease [COPD]) to see what bugs exist therein, and to also test the lungs, nasal passages and stool samples of those living in those homes, to see what bugs are similar between the microenvironments. Then, we will see if those bugs that are common to the microenvironments are those that seem to be most related to clinical features like lung function, lung inflammation, and genomic changes in the lung (this means changes in the way our genes are chemically modified and produce the proteins they are programmed to produce). If there is such a relationship, we will use these results to design interventions, such as the use of air purifiers, that may alter the relationship between the outside (air) and inner (airway) environment and then thereafter test these interventions to see if they can beneficially alter clinically meaningful parameters.

There is increasing concern over the use of e-cigarettes, also knowing as vaping, among Canadian young adults. The most recent reports indicate that young adults aged 20-24 represent one of the largest groups of e-cigarette users in Canada. Vaping may have dire and long-term consequences on the health and quality of life of young adults in Canada. In particular, because of the high concentrations of nicotine in many of the popular e-cigarette brands, the risk for nicotine addiction among this age group is high. Currently there is good evidence that vaping alone causes lung and immune function damage. Motivation for quitting vaping is difficult to improve, but some smoking literature shows that giving people feedback on their personalized health can improve motivation. In this study we will ask participants to stop vaping for 72 hours and we will measure their lung and immune function as well as their motivation for quitting vaping before and after. At the end of the 72 hours we will show participants their personal results of lung function and see if that affects their motivation for quitting vaping. We hope that this study will inform the design of a randomized controlled trial for vaping cessation because evidence is needed for clinical guidelines to help with this challenge.