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Background: Although the International Agency for Research on Cancer (IARC) has classified various indoor air pollutants as carcinogenic to humans, few studies evaluated the role of household ventilation in reducing the impact of indoor air pollutants on lung cancer risk. Objectives: To explore the association between household ventilation and lung cancer. Methods: A population-based case-control study was conducted in a Chinese population from 2003 to 2010. Epidemiologic and household ventilation data were collected using a standardized questionnaire. Unconditional logistic regression was employed to estimate adjusted odds ratios (ORadj) and their 95% confidence intervals (CI). Results: Among 1,424 lung cancer cases and 4,543 healthy controls, inverse associations were observed for good ventilation in the kitchen (ORadj = 0.86, 95% CI: 0.75, 0.98), bedroom (ORadj = 0.90, 95% CI: 0.79, 1.03), and both kitchen and bedroom (ORadj = 0.87, 95% CI: 0.75, 1.00). Stratified analyses showed lung cancer inversely associated with good ventilation among active smokers (ORadj = 0.85, 95% CI: 0.72, 1.00), secondhand smokers at home (ORadj = 0.77, 95% CI: 0.63, 0.94), and those exposed to high-temperature cooking oil fumes (ORadj = 0.82, 95% CI: 0.68, 0.99). Additive interactions were found between household ventilation and secondhand smoke at home as well as number of household pollutant sources. Conclusions: A protective association was observed between good ventilation of households and lung cancer, most likely through the reduction of exposure to indoor air pollutants, indicating ventilation may serve as one of the preventive measures for lung cancer, in addition to tobacco cessation. [ABSTRACT FROM AUTHOR]

Background & Aims: The potential interaction between family history of liver cancer and HBV infection on liver cancer has not been fully examined. Methods: We conducted a population‐based case‐control study composed of 2011 liver cancer cases and 7933 controls in Jiangsu province, China from 2003 to 2010. Data on major risk or protective factors were collected and HBV/HCV sero‐markers were assayed using blood samples. Semi‐Bayes (SB) adjustments were applied to provide posterior estimates. Results: Both family history of liver cancer (adjusted odds ratios [OR]: 4.32, 95% confidence intervals [CI]: 3.25‐5.73) and hepatitis B surface antigen (HBsAg) positivity (adjusted OR: 9.94, 95% CI: 8.33‐11.87) were strongly associated with liver cancer development. For individuals with different combinations of serological markers, the adjusted ORs were 8.45 (95% CI: 5.16‐13.82) for HBsAg‐ and HBcAb‐positive; 7.57 (95% CI: 4.87‐11.77) for HBsAg‐, HBeAg‐ and HBcAb‐positive; and 3.62 (95% CI: 2.47‐5.31) for HBsAg‐, HBeAb‐ and HBcAb‐positive, compared to all negatives in HBV serological markers. One log increase in HBV DNA level was associated with 17% increased risk (adjusted OR: 1.17, 95% CI: 1.03‐1.32). The SB‐adjusted OR of HBV‐positive individuals with family history of liver cancer was 41.34 (95% posterior interval [PI]: 23.69‐72.12) compared with those HBV‐negative without family history. Relative excess risk due to additive interaction, the attributable proportion and synergy index were 73.13, 0.87 and 8.04 respectively. Adjusted ratio of OR for multiplicative interaction was 2.84 (95% CI: 1.41‐5.75). Conclusions: Super‐additive and super‐multiplicative interactions may exist between family history of liver cancer and HBV infection on the development of liver cancer. [ABSTRACT FROM AUTHOR]

Abstract: A population-based case-control study was conducted in a high-risk area (Dafeng) and a low-risk area (Ganyu) of Jiangsu province, China. In this analysis, the population attributable fraction (PAF) was calculated to quantify the etiology of risk factors; the relative attributable risk (RAR) was applied to explore how much of the incidence difference could be explained by variations in the distribution of risk factors. Results showed that unhealthy lifestyles accounted for a high fraction of esophageal cancer in China. Dissimilar distribution of several lifestyle factors, together with hereditary variations may be largely responsible for the incidence difference between areas. [Copyright &y& Elsevier]