Lung Cancer and Cardiovascular Disease Mortality Associated with Ambient Air Pollution and Cigarette Smoke: Shape of the Exposure–Response Relationships

By C. Pope, Richard T. Burnett, Michelle C. Turner, A. Cohen, D. Krewski, Michael Jerrett, S. Gapstur, M. Thun. Environmental Health Perspectives, 2011

732 citations recorded by the source corpus.

Background: Lung cancer and cardiovascular disease (CVD) mortality risks increase with smoking, secondhand smoke (SHS), and exposure to fine particulate matter < 2.5 μm in diameter (PM2.5) from ambient air pollution. Recent research indicates that the exposure–response relationship for CVD is nonlinear, with a steep increase in risk at low exposures and flattening out at higher exposures. Comparable estimates of the exposure–response relationship for lung cancer are required for disease burden estimates and related public health policy assessments. Objectives: We compared exposure–response relationships of PM2.5 with lung cancer and cardiovascular mortality and considered the implications of the observed differences for efforts to estimate the disease burden of PM2.5. Methods: Prospective cohort data for 1.2 million adults were collected by the American Cancer Society as part of the Cancer Prevention Study II. We estimated relative risks (RRs) for increments of cigarette smoking, adjusting for various individual risk factors. RRs were plotted against estimated daily dose of PM2.5 from smoking along with comparison estimates for ambient air pollution and SHS. Results: For lung cancer mortality, excess risk rose nearly linearly, reaching maximum RRs > 40 among long-term heavy smokers. Excess risks for CVD mortality increased steeply at low exposure levels and leveled off at higher exposures, reaching RRs of approximately 2–3 for cigarette smoking. Conclusions: The exposure–response relationship associated with PM2.5 is qualitatively different for lung cancer versus cardiovascular mortality. At low exposure levels, cardiovascular deaths are projected to account for most of the burden of disease, whereas at high levels of PM2.5, lung cancer becomes proportionately more important.

Subfields: Health, Toxicology and Mutagenesis, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/42fa680ab33f5afa9c1a7bc148e49008aa2adc30

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Citations in the corpus

• Estimated Global Mortality Attributable to Smoke from Landscape Fires (2012, methodology): “Although there is increasing evidence of a log-linear association for cardiovascular mortality related to urban air pollution (Pope et al. 2011), we used the linear assumption for the principal nalysis because studies on the .cardiovascular effects of LFS have been inconclusive.”
• The Cerebellum, Sensitive Periods, and Autism (2014, background): “As a point of quantitative comparison, cigarette smoking increases the risk of lung cancer by a factor of 20 to 40 (Pope et al., 2011).”
• Household electrification and indoor air pollution (2017, unknown): “However, Pope III et al. (2011) presents an estimate of a”
• Airports, Air Pollution, and Contemporaneous Health (2016, unknown): “(2009) and Pope III et al. (2011)).”
• An Integrated Risk Function for Estimating the Global Burden of Disease Attributable to Ambient Fine Particulate Matter Exposure (2014, unknown): “• The RR of mortality from chronic disease experienced by people exposed to AAP, SHS, HAP, and AS is a function of long-term, cumulative exposure quantified in terms of daily average exposure concentration and does not depend on the temporal pattern of exposure (Pope et al. 2011a, 2011b).”
• Global premature mortality due to anthropogenic outdoor air pollution and the contribution of past climate change (2013, background): “5 and mortality may flatten at high concentrations (Pope et al 2011), suggesting that we may overestimate PM2.”
• Addressing Global Mortality from Ambient PM2.5. (2015, background): “…C-R models yield implausibly high estimates of relative risk (e.g., RR ≫ 2) for high concentrations.16−18 Instead, Burnett et al. (2014),16 building on Pope et al. (2009, 2011),17,18 developed integrated exposure-response functions (IERs) that constrain the shape of the C-R relationship using…”