DE 2 & 3 STUDY – EFFECTS OF EXPOSURE TO ALLERGENS AND AIR POLLUTION ON LUNG FUNCTION AND IMMUNITY
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).
COPA STUDY – THE EFFECTS OF TRAFFIC-RELATED AIR POLLUTION IN SMOKERS AT RISK FOR DEVELOPING CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)
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 subjects so that we may understand the very early stages of COPD development, oriented toward a framework of protection and prevention.
PAIR STUDY – EFFECTS OF PHTHALATE INHALATION ON AIRWAY IMMUNOLOGY: A CONTROLLED HUMAN EXPOSURE STUDY
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.
IDEA STUDY – THE EFFECTS OF AIR POLLUTION AND INHALED SALBUTAMOL ON LUNG FUNCTION AND ATHLETIC PERFORMANCE IN ASTHMATIC INDIVIDUALS (Collaboration project with Dr. Koehle’s lab)
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.