R M Harrison1, D J T Smith, A J Kibble. 1. Division of Environmental Health & Risk Management, The University of Birmingham, Edgbaston, Birmingham B15 2TT, UK. r.m.harrison.ipe@bham.ac.uk
Abstract
AIMS: To test whether exposure to known chemical carcinogens in the atmosphere is capable of explaining the association between concentrations of PM2.5 and lung cancer mortality observed in the extended ACS Cohort Study. METHODS: Taking account of possible cancer latency periods, lung cancer rates due to exposure to As, Cr(VI), Ni, and polycyclic aromatic hydrocarbons (PAHs) were calculated based on a review of historic measurements from the United States and the use of unit risk factors. The predicted rates were compared with rates of cancer attributable to PM2.5 derived from data in the ACS study. RESULTS: Despite many uncertainties, the lung cancer rates predicted due to exposure to US urban concentrations of the carcinogenic substances arsenic, nickel, chromium, and PAHs measured in 1960 and earlier (and hence allowing for a latency period) were within the range predicted on the basis of the ACS Cohort Study due to exposure of PM2.5. There are, however, many caveats, most particularly that for the chemical carcinogens to be responsible for the effects attributed to PM2.5 by Pope and colleagues, the concentrations of chemical carcinogens at the time of relevant exposures would need to be correlated with the concentrations of PM2.5 in US urban areas measured between 1979 and 2000 and used in the ACS study. CONCLUSIONS: While many uncertainties remain, it appears plausible that known chemical carcinogens are responsible for the lung cancers attributed to PM2.5 exposure in the extended ACS Cohort Study. However, the possibility should not be ruled out that particulate matter is capable of causing lung cancer independent of the presence of known carcinogens.
AIMS: To test whether exposure to known chemical carcinogens in the atmosphere is capable of explaining the association between concentrations of PM2.5 and lung cancer mortality observed in the extended ACS Cohort Study. METHODS: Taking account of possible cancer latency periods, lung cancer rates due to exposure to As, Cr(VI), Ni, and polycyclic aromatic hydrocarbons (PAHs) were calculated based on a review of historic measurements from the United States and the use of unit risk factors. The predicted rates were compared with rates of cancer attributable to PM2.5 derived from data in the ACS study. RESULTS: Despite many uncertainties, the lung cancer rates predicted due to exposure to US urban concentrations of the carcinogenic substances arsenic, nickel, chromium, and PAHs measured in 1960 and earlier (and hence allowing for a latency period) were within the range predicted on the basis of the ACS Cohort Study due to exposure of PM2.5. There are, however, many caveats, most particularly that for the chemical carcinogens to be responsible for the effects attributed to PM2.5 by Pope and colleagues, the concentrations of chemical carcinogens at the time of relevant exposures would need to be correlated with the concentrations of PM2.5 in US urban areas measured between 1979 and 2000 and used in the ACS study. CONCLUSIONS: While many uncertainties remain, it appears plausible that known chemical carcinogens are responsible for the lung cancers attributed to PM2.5 exposure in the extended ACS Cohort Study. However, the possibility should not be ruled out that particulate matter is capable of causing lung cancer independent of the presence of known carcinogens.
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