Air pollution and cancer: biomarker studies in human populations †

Abstract

Large cohort studies in the U.S. and in Europe suggest that air pollution may increase lung cancer risk. Biomarkers can be useful to understand the mechanisms and to characterize high-risk groups. Here we describe biomarkers of exposure, in particular DNA adducts as well as markers of early damage, including mutagenicity, other endpoints of genotoxicity and molecular biomarkers of cancer. Several studies found an association between external measures of exposure to air pollution and increased levels of DNA adducts, with an apparent levelling-off of the dose-response relationship. Also, numerous experimental studies in vitro and in vivo have provided unambiguous evidence for genotoxicity of air pollution. In addition, due to the organic extracts of particulate matter [especially various polycyclic aromatic hydrocarbon (PAH) compounds], particulate air pollution induces oxidative damage to DNA. The experimental work, combined with the data on frequent oxidative DNA damage in lymphocytes in people exposed to urban air pollution, suggests 8-oxo-dG as one of the important promutagenic lesions. Lung cancer develops through a series of progressive pathological changes occurring in the respiratory epithelium. Molecular alterations such as loss of heterozygosity, gene mutations and aberrant gene promoter methylation have emerged as potentially promising molecular biomarkers of lung carcinogenesis. Data from such studies relevant for emissions rich in PAHs are also summarized, although the exposure circumstances are not directly relevant to outdoor air pollution, in order to shed light on potential mechanisms of air pollution-related carcinogenesis.

The relationship between biomarkers of oxidative DNA damage, polycyclic aromatic hydrocarbon DNA adducts, antioxidant status and genetic susceptibility following exposure to environmental air pollution in humans

“…There is evidence that populations exposed to urban pollution show increased levels of polycyclic aromatic hydrocarbon (PAH) DNA adducts, supporting the hypothesis that PAHs are significant contributors to the genotoxicity and carcinogenicity of air pollution in the urban environment [1], [2] and [3]. Examples include DNA samples from bus drivers in Copenhagen [4], and from populations living in regions with increased pollution in Czech Republic [5] and [6], and Poland [7].…”

Fruit and vegetable intake influences the association between exposure to polycyclic aromatic hydrocarbons and a marker of oxidative stress in pregnant women

“…Polycyclic aromatic hydrocarbons (PAHs) are a family of chemicals that are produced because of the incomplete combustion of organic products and are significant contributors to the carcinogenicity of air pollution (Peluso et al, 2001;Castaño-Vinyals et al, 2004;Vineis and Husgafvel-Pursiainen, 2005). Humans are exposed to PAHs through a variety of sources, including occupational exposure, smoking, diet, drinking water and outdoor/indoor air particulates (Lijinsky, 1991;Ovrebø et al, 1992;Kang et al, 2005).…”

Evaluation of The Diagnostic Role of Non-Coding RNA and Exosomal Related Gene Association in Lung Cancer

“…The long-term of surrounding air pollution as exposure to various polycyclic aromatic hydrocarbon compounds is associated with the risk of lung cancer, most probably by inflammation, oxidative stress, stimulation of a procoagulatory state and disturbance of the autonomic nervous system (9) . It is estimated that 11% of lung cancers are attributed to urban air pollution among Europeans (10) .…”