Lung cancer, chronic obstructive pulmonary disease and air pollution.
- Author:
Joo Hon SUNG
1
;
Soo Hun CHO
;
Dae Hee KANG
;
Keun Young YOO
Author Information
1. Department of Preventive Medicine, Seoul National University College of Medicine, Korea.
- Publication Type:Original Article
- Keywords:
Air Pollution;
Lung Cancer;
COPD;
Smoking
- MeSH:
Air Pollutants;
Air Pollution*;
Asthma;
Bronchitis, Chronic;
Cardiovascular Diseases;
Case-Control Studies;
Cohort Studies;
Information Storage and Retrieval;
Environmental Monitoring;
Heart;
Heart Failure;
Humans;
Insurance;
Korea;
Logistic Models;
Lung Diseases, Obstructive;
Lung Neoplasms*;
Lung*;
Motor Vehicles;
Physical Examination;
Pulmonary Disease, Chronic Obstructive*;
Surveys and Questionnaires;
Smoke;
Smoking
- From:Korean Journal of Preventive Medicine
1997;30(3):585-598
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Although there are growing concerns about the adverse health effect of air pollution, not much evidence on health effect of current air pollution level had been accumulated yet in Korea. This study was designed to evaluate the chronic health effect of air pollution using Korean Medical Insurance Corporation (KMIC) data and air quality data. Medical insurance data in Korea have some drawback in accuracy, but they do have some strength especially in their national coverage, in having unified ID system and individual information which enables various data linkage and chronic health effect study. METHOD: This study utilized the data of Korean Environmental Surveillance System Study (Surveillance Study), which consist of asthma, acute bronchitis, chronic obstructive pulmonary diseases (COPD), cardiovascular diseases (congestive heart failure and ischemic heart disease), all cancers, accidents and congenital anomaly, i.e., mainly potential environmental diseases. We reconstructed a nested case-control study with Surveillance Study data and air pollution data in Korea. Among 1,037,210 insured who completed questionnaire and physical examination in 1992, disease free (for chronic respiratory disease and cancer) persons, between the age of 35-64 with smoking status information were selected to reconstruct cohort of 564,991 persons. The cohort was followed-up to 1995 (1992-5) and the subjects who had the diseases in Surveillance Study were selected. Finally, the patients, with address information and available air pollution data, left to be 'final subjects'. Cases were defined to all lung cancer cases (424) and COPD admission cases (89), while control groups are determined to all other patients than two case groups among 'final subjects'. That is, cases are probable chronic environmental diseases, while controls are mainly acute environmental diseases. For exposure, Air quality data in 73 monitoring sites between 1991 - 1993 were analyzed to surrogate air pollution exposure level of located areas (58 areas). Five major air pollutants data, TSP, O3, SO2, CO, NOx was available and the area means were applied to the residents of the local area. 3-year arithmetic mean value, the counts of days violating both long-term and shot-term standards during the period were used as indices of exposure. Multiple logistic regression model was applied. All analyses were performed adjusting for current and past smoking history, age, gender. Results: Plain arithmetic means of pollutants level did not succeed in revealing any relation to the risk of lung cancer or COPD, while the cumulative counts of non-attainment days did. All pollutants indices failed to show significant positive findings with COPD excess. Lung cancer risks were significantly and consistently associated with the increase of O3and CO exceedance counts(to corrected error level - 0.017) and less strongly and consistently with SO2 and TSP. SO2and TSP showed weaker and less consistent relationship. O3and CO were estimated to increase the risks of lung cancer by 2.04 and 1.46 respectively, the maximal probable risks, derived from comparing more polluted area (95%) with cleaner area (5%). CONCLUSIONS: Although not decisive due to potential misclassication of exposure, these results were drawn by relatively conservative interpretation, and could be used as an evidence of chronic health effect especially for lung cancer. O3might be a candidate for promoter of lung cancer, while CO should be considered as surrogated measure of motor vehicle emissions. The control selection in this study could have been less appropriate for COPD, and further evaluation with another setting might be necessary.
