Polycyclic aromatic hydrocarbon (PAH) exposure study in China

August 21, 2009 · 0 comments

Cancer Epidemiol Biomarkers Prev. 2009 Aug 18.

Aryl Hydrocarbon Receptor Expression Is Associated with a Family History of Upper Gastrointestinal Tract Cancer in a High-Risk Population Exposed to Aromatic Hydrocarbons.

Roth MJ, Wei WQ, Baer J, Abnet CC, Wang GQ, Sternberg LR, Warner AC, Johnson LL, Lu N, Giffen CA, Dawsey SM, Qiao YL, Cherry J.

1Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute; 2National Center for Complementary and Alternative Medicine, National Institutes of Health, Bethesda, Maryland; Departments of 3Cancer Epidemiology, 4Endoscopy, and 5Pathology, Cancer Institute, Chinese Academy of Medical Sciences, Beijing, People’s Republic of China; 6Laboratory of Molecular Technology and 7Pathology and Histotechnology Laboratory, Science Applications International Corporation-Frederick, Inc., National Cancer Institute-Frederick, Frederick, Maryland; and 8Information Management Services, Silver Spring, Maryland.

BACKGROUND: Polycyclic aromatic hydrocarbon (PAH) exposure is a risk factor for esophageal squamous cell carcinoma, and PAHs are ligands of the aryl hydrocarbon receptor (AhR). This study measured the expression of AhR and related genes in frozen esophageal cell samples from patients exposed to different levels of indoor air pollution, who did or did not have high-grade squamous dysplasia and who did or did not have a family history of upper gastrointestinal tract (UGI) cancer.

METHODS: 147 samples were evaluated, including 23 (16%) from patients with high-grade dysplasia and 48 (33%) from patients without dysplasia who heated their homes with coal, without a chimney (a “high” indoor air pollution group), and 27 (18%) from patients with high-grade dysplasia and 49 (33%) from patients without dysplasia who did not heat their homes at all (a “low” indoor air pollution group). Sixty-four (44%) had a family history of UGI cancer. RNA was extracted and quantitative PCR analysis was done.

RESULTS: AhR gene expression was detectable in 85 (58%) of the samples and was >9-fold higher in those with a family history of UGI cancer [median expression (interquartile range), -1,964 (-18,000, -610) versus -18,000 (-18,000, -1036); P = 0.02, Wilcoxon rank-sum test]. Heating status, dysplasia category, age, gender, and smoking were not associated with AhR expression (linear regression; all P values >/= 0.1).

CONCLUSION: AhR expression was higher in patients with a family history of UGI cancer. Such individuals may be more susceptible to the deleterious effects of PAH exposure, including PAH-induced cancer. (Cancer Epidemiol Biomarkers Prev 2009;18(9):OF1-6).

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