Public Lecture by Wei Lun Visiting Professor

A Biographical Sketch

Professor David Christiani is Professor of Occupational Medicine and Epidemiology at Harvard School of Public Health, Professor of Medicine at Harvard Medical School , and Physician at Massachusetts General Hospital in Boston, USA.

He received his MD from Tufts University and his MS and MPH from the Harvard School of Public Health.

Professor Christiani's major research interests are environmental molecular epidemiology, specifically gene-environment interactions. He has studied the impact of exposure to various pollutants on health and the interactions between host factors (genetic and acquired susceptibility), and environmental exposure in producing acute and chronic diseases. This research is part of an emerging field known as molecular epidemiology. Professor Christiani has developed new methods for assessing health effects after exposure to carcinogens and other toxicants . He has a very active interest in international occupational and environmental health studies.

Professor Christiani has developed and applied new biologic markers used in examination of pollutant-induced diseases such as lung cancer, bladder cancer, skin cancer and upper respiratory-tract inflammation. He has led a large NIH-funded multidisciplinary study of the molecular and genetic analysis of lung cancer with specific attention to genetic susceptibility to lung cancer and genetic predictors of treatment outcomes. This research has worked as a model for examining gene-environmental interactions for cancer development.

He has also initiated a project that examines respiratory effects of exposure to respiratory toxins contained in particles from fossil-fuel burning power plants. The study involves an epidemiologic evaluation of the acute respiratory effects of exposure as well as a detailed investigation including examination of molecular markers in nasal fluid and lung lavage fluid in exposed workers and controls.

In February, 2000 Professor Christiani received an award from NIH to study the molecular epidemiology of acute lung injury and Acute Respiratory Distress Syndrome (ARDS), a disorder that occurs after a toxic insult to the lung (e.g., sepsis, smoke inhalation). The syndrome has a high associated mortality, and little is known to prevent its development.

On the international scene, Professor Christiani has led a 27-year longitudinal study of respiratory diseases in cotton-textile workers in Shanghai. The objectives of the study include determining the rate of loss in lung function among cotton dust-exposed workers at various levels of dust exposure and evaluating the relationship of exposure to gram-negative bacterial endotoxin and acute and chronic lung diseases . Professor Christiani and his team have expanded the study to include an assessment of relevant genetic factors, and an examination of reproductive effects of shift work and ergonomic factors at work as well as the exposures noted above.

Professor Christiani has conducted biomedical research on three continents: Asia, Africa, and Central America. He has developed a wide network of collaboratives and contacts as he undertakes new studies of the reproductive effects of exposure to chemicals ( mainland China), arsenic exposure and bladder and skin cancer (Taiwan and Bangladesh), exposure to indoor combustion products in respiratory diseases (Central America), petrochemical exposures, brain neoplasms and leukemia in Asia (Taiwan), and respiratory effects of paraquat exposure (Africa). An exciting aspect of the international work is in methodology, specifically, the development and adaptation of epidemiologic and laboratory techniques to the conditions of the industrializing world. The potential for effective interventions for disease prevention makes this work particularly rewarding.

Synopsis of the Lecture

Although up to 90% of lung cancer in the United States is attributed to cigarette smoking, only 10% of smokers develop bronchogenic carcinoma. An explanation for this observation is that host factors influence individual susceptibility to tobacco smoke. One such susceptibility factor is the group of pleiotropic genes that control activation (Phase I) and detoxification (Phase II) of potential carcinogens. Metabolism of environmental compounds may alter the lipophilic properties of a molecule, or more subtly introduce electronegative moieties within the molecule, influencing its carcinogenic potential. In humans a significant proportion of xenobiotic metabolizing enzymes is polymorphic. Other susceptibility factors are related to defects in DNA repair, alterations in tumor suppressor genes, angiogenesis, and alterations in tumor invasiveness factors. Polymorphisms in genes associated with these functions also may be involved in lung cancer development.

The aim of this presentation is to describe the role of inherited polymorphisms of genes involved in xenobiotic metabolism, DNA repair, and tumor suppression/invasion (alone and in combination) in lung cancer risk, and modification of this risk by environmental factors such as smoking and diet. In addition, recent data from genome-wide association studies (GWAS) of both lung cancer risk and outcomes will be described.

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