title: Household endotoxin levels and the risk of non-Hodgkin lymphoma.
abstract: OBJECTIVE
  Endotoxin, a component of the outer membrane of gram-negative bacteria, elicits a strong innate and inflammatory immune response associated with the secretion of proinflammatory cytokines, including tumor necrosis factor-alpha (TNF-α). Because TNF-α polymorphisms that increase TNF-α production are associated with an increased risk of non-Hodgkin lymphoma (NHL), we hypothesized that increased levels of household endotoxin would be associated with an increased NHL risk.
  
  
  METHODS
  We evaluated this association in the National Cancer Institute/Surveillance, Epidemiology and End Results (NCI/SEER) NHL multicenter population-based case-control study. Used vacuum cleaner bags were collected from participants during a home interview. Dust samples from the bags of 594 cases and 442 controls were analyzed for endotoxin [endotoxin unit (EU)/mg of dust] using the kinetic chromogenic Limulus amebocyte lysate assay. Multivariable logistic regression was used to estimate the effect of endotoxin on NHL risk adjusted for age, sex, race, education, study center, and farm exposure.
  
  
  RESULTS
  Endotoxin was not associated with NHL overall [odds ratio (OR) for highest quartile of endotoxin levels = 0.81, 95 % confidence interval (CI) = 0.55, 1.20; p for trend = 0.35] or with diffuse large B-cell lymphoma (OR = 0.63, 95 % CI = 0.34, 1.16; p = 0.31) or follicular lymphoma (OR = 1.07, 95 % CI = 0.61, 1.89; p = 0.73) subtypes. Both working and living on a farm were associated with higher household endotoxin levels compared to never working (p = 0.009) or living (p = 0.01) on a farm. Excluding farmers from the analysis did not change the results.
  
  
  CONCLUSIONS
  We found no evidence of a role for household endotoxin in NHL etiology.
authors.affiliation: Department of Preventive Medicine, USC Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
authors.forename: Jun
authors.initials: J
authors.lastname: Wang
authors.forename: Wendy
authors.initials: W
authors.lastname: Cozen
authors.forename: Peter S
authors.initials: PS
authors.lastname: Thorne
authors.forename: Kiros
authors.initials: K
authors.lastname: Berhane
authors.forename: James R
authors.initials: JR
authors.lastname: Cerhan
authors.forename: Patricia
authors.initials: P
authors.lastname: Hartge
authors.forename: Mary H
authors.initials: MH
authors.lastname: Ward
authors.forename: Anneclaire J
authors.initials: AJ
authors.lastname: De Roos
authors.forename: Richard K
authors.initials: RK
authors.lastname: Severson
authors.forename: Lindsay M
authors.initials: LM
authors.lastname: Morton
authors.forename: Leslie
authors.initials: L
authors.lastname: Bernstein
authors.forename: Martha S
authors.initials: MS
authors.lastname: Linet
authors.forename: Joanne S
authors.initials: JS
authors.lastname: Colt
mesh_terms: D000368:Aged; D016022:Case-Control Studies; D004731:Endotoxins / Q000506:poisoning*; D004781:Environmental Exposure / Q000009:adverse effects*; D005191:Family Characteristics; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D008228:Lymphoma, Non-Hodgkin / Q000139:chemically induced / Q000453:epidemiology* / Q000235:genetics; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D018426:SEER Program; D014481:United States / Q000453:epidemiology
chemical_list: D004731:Endotoxins