Outdoor air pollution exposures and incident cancer risk in the PLCO cohort
Principal Investigator
Name
Rena Jones
Degrees
Ph.D., M.S.
Institution
National Cancer Institute
Position Title
Investigator
Email
About this CDAS Project
Study
PLCO
(Learn more about this study)
Project ID
PLCO-947
Initial CDAS Request Approval
Mar 22, 2022
Title
Outdoor air pollution exposures and incident cancer risk in the PLCO cohort
Summary
The International Agency for Research on Cancer has classified ambient air pollution, specifically PM, as a Group 1 carcinogen largely based on evidence of lung carcinogenicity [1]. However, studies investigating whether long-term exposure to elevated fine particulate matter less than 2.5 microns in diameter (i.e., PM_{2.5}) concentrations is associated with cancer risks remain fairly limited, especially for organ sites other than the lung. Also of interest is the effect of PM_{2.5} chemical components (e.g., carbon, nitrate, sulfate) on cancer risk. PM_{2.5} cytotoxicity has been demonstrated via multiple pathways [2], suggesting the potential importance of specific PM_{2.5} components. However, it is unknown whether these components contribute to cancer or whether differential exposure to individual PM_{2.5} components may contribute to etiologic heterogeneity for cancers.
The PLCO study provides a geographically widespread U.S. cohort in which to explore PM_{2.5}-cancer associations, affording heterogeneity in PM_{2.5} concentrations coupled with large numbers of incident cancer cases. As ambient PM_{2.5} levels are likely to have a modest impact on cancer relative to health behaviors such as smoking, it is crucial to control for these factors as individual confounders. The rich cohort dataset will be useful in this regard, with available data on smoking history, dietary and lifestyle factors, and hormonal exposures. Weaknesses of prior studies of incident cancer risk may also be addressed, such as the ability to examine residential mobility as a potential source of exposure misclassification. Annual modeled estimates of outdoor PM_{2.5} total mass and components, nitrogen dioxide (NO_{2}), and ozone (O_{3}) have been previously linked to geocoded cohort participant residences (N=92,353 participants with available residential histories) at various spatial scales (ranging from census tract to grids up to 36 kilometers). For each participant, we will generate a long-term average exposure estimate based on the temporal availability of the data, which varies for each pollutant, starting with the earliest available year of data (PM_{2.5}: 2000-2017; NO_{2}: 2000-2010; O_{3}: 2002-2016).
References
1. Loomis D, Grosse Y, Lauby-Secretan B, El Ghissassi F, Bouvard V, Benbrahim-Tallaa L, Guha N, Baan R, Mattock H, Straif K, International Agency for Research on Cancer Monograph Working Group IARC. The carcinogenicity of outdoor air pollution. Lancet Oncol 2013;14:1262–3.
2. Bekki K, Ito T, Yoshida Y, He C, Arashidani K, He M, Sun G, Zeng Y, Sone H, Kunugita N, Ichinose T. PM 2.5 collected in China causes inflammatory and oxidative stress responses in macrophages through the multiple pathways. Environmental Toxicology and Pharmacology 2016;45:362–9.
The PLCO study provides a geographically widespread U.S. cohort in which to explore PM_{2.5}-cancer associations, affording heterogeneity in PM_{2.5} concentrations coupled with large numbers of incident cancer cases. As ambient PM_{2.5} levels are likely to have a modest impact on cancer relative to health behaviors such as smoking, it is crucial to control for these factors as individual confounders. The rich cohort dataset will be useful in this regard, with available data on smoking history, dietary and lifestyle factors, and hormonal exposures. Weaknesses of prior studies of incident cancer risk may also be addressed, such as the ability to examine residential mobility as a potential source of exposure misclassification. Annual modeled estimates of outdoor PM_{2.5} total mass and components, nitrogen dioxide (NO_{2}), and ozone (O_{3}) have been previously linked to geocoded cohort participant residences (N=92,353 participants with available residential histories) at various spatial scales (ranging from census tract to grids up to 36 kilometers). For each participant, we will generate a long-term average exposure estimate based on the temporal availability of the data, which varies for each pollutant, starting with the earliest available year of data (PM_{2.5}: 2000-2017; NO_{2}: 2000-2010; O_{3}: 2002-2016).
References
1. Loomis D, Grosse Y, Lauby-Secretan B, El Ghissassi F, Bouvard V, Benbrahim-Tallaa L, Guha N, Baan R, Mattock H, Straif K, International Agency for Research on Cancer Monograph Working Group IARC. The carcinogenicity of outdoor air pollution. Lancet Oncol 2013;14:1262–3.
2. Bekki K, Ito T, Yoshida Y, He C, Arashidani K, He M, Sun G, Zeng Y, Sone H, Kunugita N, Ichinose T. PM 2.5 collected in China causes inflammatory and oxidative stress responses in macrophages through the multiple pathways. Environmental Toxicology and Pharmacology 2016;45:362–9.
Aims
We aim to assess the association between outdoor air pollutants, specifically PM_{2.5} concentrations and its components, and cancer risk in the PLCO cohort. We will initially focus on cancer overall and major organ sites with the strongest a priori hypotheses for associations (e.g., lung, bladder, lymphohematopoietic, breast, and gastrointestinal cancers).
Collaborators
Jared Fisher (NIH/NCI/DCEG/OEEB), Samantha Ammons (NIH/NCI/DCEG/OEEB), Jongeun Rhee (NIH/NCI/DCEG/OEEB), Wen-Yi Huang (NIH/NCI/DCEG/MEB), Neal Freedman (NIH/NCI/DCEG/MEB), Rena Jones (NIH/NCI/DCEG/OEEB)