PM10-bound polycyclic aromatic hydrocarbons: Biological indicators, lung cancer risk of realistic receptors and ‘source-exposure-effect relationship’ under different source scenarios

• Published in: Chemosphere (Oxford) 2012-06, Vol.87 (11), p.1381-1387
• Main Authors: Wickramasinghe, A.P., Karunaratne, D.G.G.P., Sivakanesan, R.
• Format: Article
• Language: English
• Subjects: Benzo(a)pyrene (B[a]P); Biological and medical sciences; Biological indicators; Chemical and industrial products toxicology. Toxic occupational diseases; Environmental and health policy; Lung cancer risk; Medical sciences; Polycyclic aromatic hydrocarbons (PAHs); Source scenarios; Toxicology; Various organic compounds
• ISSN: 0045-6535; 1879-1298
• DOI: 10.1016/j.chemosphere.2012.02.044

► The record of a total profile of all carcinogens are important in PAH cancer studies. ► B[a]P is not the sole indicator for the carcinogenic risk of ambient air PAHs. ► D[ah]A is a better co-indicator for the community PAHs exposure studies. ► Generally, ∑p-PAHs show strong correlation (r=0.8) to the predicted risk levels. ► Cancer risk does not correlate well with traffic volume, but does with firewood use. Cancer has become a critical health issue in the world heritage city Kandy, Sri Lanka. Polycyclic aromatic hydrocarbons (PAHs), one of persistent organic pollutants, in the atmosphere may be a major etiological factor in lung carcinogenicity. Over the very high concentrations of ambient air PAHs reported in Kandy, this paper is focused on setting priorities to control human exposure to PAHs in prevention of cancer. On re-appraisal of the classical indicator benzo(a)pyrene (B[a]P) for atmospheric PAHs-related carcinogenicity, B[a]P failed to reflect the toxicity completely and may not be the sole indicator for risk assessment studies in complex multi-sourced urban environments. The excess lifetime lung cancer risks of atmospheric PAHs with ‘less than lifetime exposure’ were assessed based on both ‘B[a]P toxic equivalents’ and ‘B[a]P surrogate epidemiological’ approach of risk quantification, over emissions characterized urban, suburban, and rural areas of Kandy. In urban heavy traffic areas, PAH-related additional cancer burden has been 942million−1 over 30y of exposure. Over the whole study area, ∑p-PAHs show strong correlation (r=0.8) to the predicted risk levels. While the urban and suburban predicted cancer risk levels could not show significant correlation to their emission sources indicating the real complexity in mega urban environments, the rural lung cancer risk levels correlated perfectly with the source, firewood combustion. Policy decisions on environment and health could be based on established correlations among ‘emission sources-exposures-health effects’. The priority for “analysis of options and policy formulation to reduce inhalation PAHs exposure of population in Kandy” was considered “moderate to high”.