PM2.5, vegetation density, and childhood cancer: a case-control registry-based study from Texas 1995-2011

Author:

Williams Lindsay A123ORCID,Haynes David4ORCID,Sample Jeannette M1,Lu Zhanni1,Hossaini Ali4,McGuinn Laura A5,Hoang Thanh T678,Lupo Philip J678,Scheurer Michael E678ORCID

Affiliation:

1. Division of Epidemiology and Clinical Research, Department of Pediatrics, University of Minnesota , Minneapolis, MN, USA

2. Masonic Cancer Center, University of Minnesota , Minneapolis, MN, USA

3. Brain Tumor Program, University of Minnesota , Minneapolis, MN, USA

4. Institute for Health Informatics, University of Minnesota , Minneapolis, MN, USA

5. Department of Family Medicine, University of Chicago , Chicago, IL, USA

6. Department of Pediatrics, Division of Hematology-Oncology, Baylor College of Medicine , Houston, TX, USA

7. Dan L. Duncan Comprehensive Cancer Center, Baylor College of Medicine , Houston, TX, USA

8. Cancer and Hematology Center, Texas Children’s Hospital , Houston, TX, USA

Abstract

Abstract Background Air pollution is positively associated with some childhood cancers, whereas greenness is inversely associated with some adult cancers. The interplay between air pollution and greenness in childhood cancer etiology is unclear. We estimated the association between early-life air pollution and greenness exposure and childhood cancer in Texas (1995 to 2011). Methods We included 6101 cancer cases and 109 762 controls (aged 0 to 16 years). We linked residential birth address to census tract annual average fine particulate matter <2.5 µg/m³ (PM2.5) and Normalized Difference Vegetation Index (NDVI). We estimated odds ratios (ORs) and 95% confidence intervals (CIs) between PM2.5/NDVI interquartile range increases and cancer. We assessed statistical interaction between PM2.5 and NDVI (likelihood ratio tests). Results Increasing residential early-life PM2.5 exposure was associated with all childhood cancers (OR = 1.10, 95% CI = 1.06 to 1.15), lymphoid leukemias (OR = 1.15, 95% CI = 1.07 to 1.23), Hodgkin lymphomas (OR = 1.27, 95% CI = 1.02 to 1.58), non-Hodgkin lymphomas (OR = 1.24, 95% CI = 1.02 to 1.51), ependymoma (OR = 1.27, 95% CI = 1.01 to 1.60), and others. Increasing NDVI exposure was inversely associated with ependymoma (0- to 4-year-old OR = 0.75, 95% CI = 0.58 to 0.97) and medulloblastoma (OR = 0.75, 95% CI = 0.62 to 0.91) but positively associated with malignant melanoma (OR = 1.75, 95% CI = 1.23 to 2.47) and Langerhans cell histiocytosis (OR = 1.56, 95% CI = 1.07 to 2.28). There was evidence of statistical interaction between NDVI and PM2.5 (P < .04) for all cancers. Conclusion Increasing early-life exposure to PM2.5 increased the risk of childhood cancers. NDVI decreased the risk of 2 cancers yet increased the risk of others. These findings highlight the complexity between PM2.5 and NDVI in cancer etiology.

Funder

National Institutes of Environmental Health Sciences

Publisher

Oxford University Press (OUP)

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1. The complexities of PM2.5, greenspace, and childhood cancer;JNCI: Journal of the National Cancer Institute;2024-04-19

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