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Organochlorines in Carpet Dust and Non-Hodgkin Lymphoma

Colt, Joanne S.*; Severson, Richard K.; Lubin, Jay*; Rothman, Nat*; Camann, David; Davis, Scott§; Cerhan, James R.; Cozen, Wendy; Hartge, Patricia*

doi: 10.1097/01.ede.0000164811.25760.f1
Original Article

Background: The incidence of non-Hodgkin lymphoma (NHL) has risen over the past several decades. Reasons for this increase are largely unexplained.

Methods: In this population-based case–control study, we examined NHL risk and exposure to organochlorine compounds using concentrations in carpet dust as an exposure indicator. We identified NHL cases, uninfected with HIV, diagnosed between 1998 and 2000 among women and men ages 20–74 years in Iowa, Los Angeles County, and the Detroit and Seattle metropolitan areas. Controls were selected using random-digit-dialing or Medicare files. Organochlorine concentrations were measured in vacuum bag dust from 603 white cases and 443 white controls who had owned most of their carpets for at least 5 years.

Results: NHL risk was elevated if any of the polychlorinated biphenyl (PCB) congeners (PCBs 105, 138, 153, 170, or 180) was detected (odds ratio = 1.5; 95% confidence interval = 1.2–2.0). Risk was elevated in the top tertile of PCB 180 (1.7; 1.1–2.6) and in the top 2 tertiles of total PCBs (middle tertile, 1.6 [1.1–2.4]; top tertile 1.5 [1.0–2.2]). There was a positive trend in risk with increasing PCB 180 levels (P trend = 0.03). NHL risk was elevated if dichlorodiphenyldichloroethylene (DDE) was detected (1.3; 1.0–1.7), but only among men. A positive, but not monotonic, dose–response relationship was observed for DDE (P trend = 0.02).

Conclusions: Our findings suggest an increased risk of NHL associated with exposure to PCBs, with evidence of greater effects for PCB 180. There is also some evidence of an association with DDE.

From the *Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD; the †Karmanos Cancer Institute and Department of Family Medicine, Wayne State University, Detroit, MI; the ‡Southwest Research Institute, San Antonio, TX; the §Fred Hutchinson Cancer Research Center and the University of Washington, Seattle, WA; the ∥Mayo Clinic, College of Medicine, Rochester, MN; and the ¶University of Southern California, Los Angeles, CA.

Submitted 23 April 2004; final version accepted 18 February 2005.

Funded by the following contracts with the National Cancer Institute: N01-CN-67008, N01-CN-67010, N01-PC-65064, N01-PC-67009, N02-CP-19114, and N02-CP-71105.

Supplemental material for this article is available with the online version of the journal at www.epidem.com.

Correspondence: Joanne S. Colt, National Cancer Institute, Occupational and Environmental Epidemiology Branch, 6120 Executive Boulevard, Room 8112, Rockville, MD 20852. E-mail: coltj@mail.nih.gov.

© 2005 Lippincott Williams & Wilkins, Inc.