Clinical and pathological characteristics, outcome and mutational profiles regarding non-small-cell lung cancer related to wood-smoke exposure

J Thorac Oncol. 2012 Aug;7(8):1228-34. doi: 10.1097/JTO.0b013e3182582a93.


Hypothesis: Although smoking is the major risk factor for non-small-cell lung cancer (NSCLC), other factors are also associated with lung carcinogenesis, such as wood-smoke exposure (WSE). This article has been aimed at suggesting that lung cancer related to cigarette smoking and lung cancer related to WSE have different clinical and genetic characteristics.

Experimental design: A cohort of 914 lung cancer patients was prospectively studied; they had been treated at Mexico's National Cancer Institute between 2007 and 2010. The associations of WSE and cigarette smoking with clinical characteristics, mutation profile, response to chemotherapy, and epidermal growth factor receptor tyrosine kinase inhibitors were analyzed, and overall survival (OS) rate was calculated. The trial was registered with NCT01023828.

Results: Of the lung cancer patients studied, 95.1% were classified as coming within the NSCLC histology subtype; 58% of the patients smoked cigarettes, 35% had a background of WSE (exposure to both cigarette smoke and wood smoke was documented in 12.1% of all patients), and 19.4% patients had no smoke-exposure background. WSE was associated with NSCLC and adenocarcinoma histology, and was also more frequently associated with epidermal growth factor receptor-mutations than cigarette-smoking patients were (50.0% cf. 19.4%), whereas KRAS mutations were less common in WSE patients (6.7%) than in smokers (21%). WSE patients had a higher epidermal growth factor receptor tyrosine kinase inhibitor response rate (39.7%) than smokers (18.8%). The NSCLC patient WSE group's OS was longer (22.7 months) than that for smokers (13.8 months).

Conclusion: NSCLC patients who smoked tobacco/cigarettes differed from those having a background of WSE regarding tumor histology, mutation profile, response rate, and OS, indicating that different carcinogenic mechanisms were induced by these two types of smoke exposure.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenocarcinoma / genetics
  • Adenocarcinoma / mortality
  • Adenocarcinoma / pathology
  • Carcinoma, Large Cell / genetics
  • Carcinoma, Large Cell / mortality
  • Carcinoma, Large Cell / pathology
  • Carcinoma, Non-Small-Cell Lung / genetics*
  • Carcinoma, Non-Small-Cell Lung / mortality
  • Carcinoma, Non-Small-Cell Lung / pathology*
  • Carcinoma, Squamous Cell / genetics
  • Carcinoma, Squamous Cell / mortality
  • Carcinoma, Squamous Cell / pathology
  • ErbB Receptors / genetics*
  • Female
  • Humans
  • Lung Neoplasms / genetics
  • Lung Neoplasms / mortality
  • Lung Neoplasms / pathology
  • Male
  • Middle Aged
  • Mutation / genetics*
  • Prognosis
  • Prospective Studies
  • Proto-Oncogene Proteins / genetics*
  • Proto-Oncogene Proteins p21(ras)
  • Risk Factors
  • Small Cell Lung Carcinoma / genetics
  • Small Cell Lung Carcinoma / mortality
  • Small Cell Lung Carcinoma / pathology
  • Smoke / adverse effects*
  • Survival Rate
  • Wood*
  • ras Proteins / genetics*


  • KRAS protein, human
  • Proto-Oncogene Proteins
  • Smoke
  • EGFR protein, human
  • ErbB Receptors
  • Proto-Oncogene Proteins p21(ras)
  • ras Proteins

Associated data