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.
DICE STUDY – A CONTROLLED DOSE-RESPONSE HUMAN STUDY TO DEVELOP A SIGNATURE OF OCCUPATIONAL DIESEL EXHAUST EXPOSURE
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.
DIGR STUDY – EFFECTS OF INHALED DIESEL EXHAUST ON GLUCOCORTICOID RESISTANCE
Inflammation is the body’s response to harmful things, such as pathogens or irritating chemicals, which can cause symptoms. Exposure to allergens to which an individual is sensitive also causes inflammation, which can be seen and measured in the skin during a skin prick test in which a small amount of allergen is placed on the skin and the skin pierced. Specific allergens also cause inflammation in the lungs when inhaled them by individuals who are sensitive to these allergens and have asthma, resulting in symptoms such as wheezing, chest tightness, coughing and increased sticky secretions of mucus. Lung inflammation is enhanced by exposure to air pollutants, such as wood smoke or diesel exhaust. Many asthmatics take inhaled corticosteroids to reduce the inflammation in the lungs and thereby decrease asthma symptoms. We are interested in studying the effects of an inhaled corticosteroid on lung inflammation after exposure to diesel exhaust. This research study will test whether diesel exhaust reduces the effectiveness of inhaled corticosteroids.
Interested in participating in our active studies? Please visit Study Participation.