Lina Mu

Background:Few studies have investigated environmental tobacco smoke (ETS), commonly known as secondhand smoke, and gastric cancer (GC) risk, and the findings have been inconsistent. We conducted a pooled analysis from StoP Project and a comprehensive meta-analysis to evaluate the potential impact of ETS exposure on GC risk. Methods:Five case-control studies with ETS information from the StoP project were included (1,560 GC cases and 2,497 controls). Study-specific odds ratios (ORs) and the corresponding 95% confidence intervals (CI) were estimated using unconditional logistic regression models, adjusting for potential confounders. Pooled effect estimates were computed using random-effects models, with heterogeneity assessed using I2 (%) statistics. A comprehensive meta-analysis was conducted including the StoP project and published studies (n=14), with publication bias assed via funnel plot and Egger’s test. Results:Study-specific estimates were heterogeneous, with stronger associations observed among never-smokers. A strong positive association was observed in the Iran study (aOR = 2.38; 95%CI: 1.11, 5.09) among never-smokers. ETS exposure was not associated with GC risk in the pooled StoP analysis. In the comprehensive meta-analysis, the H. pylori-adjusted subgroup showed a positive association (aOR = 1.41; 95% CI: 1.21-1.64). The overall aOR was 1.25 (95% CI: 0.98-1.59, I2 = 69.9%). Conclusions:The results support the hypothesis that ETS could be a risk factor for GC, underscoring the importance of targeted preventive measures and public health policies to reduce ETS exposure. Impact:This study provides the most comprehensive evaluation to date of ETS exposure and highlights ETS as a preventable GC risk factor.

Research on per- and polyfluoroalkyl substances (PFAS) and biomarkers potentially related to oxidative stress in adolescents is limited. We investigated associations between serum PFAS and total bilirubin and albumin among 1474 participants aged 12–20 years using National Health and Nutrition Examination Survey 2011–2018 data. Six primary PFAS and two secondary measures, summed branched perfluorooctanesulfonic acid (Sm-PFOS) and total PFOS, were assessed. Survey-weighted linear regression with multiple imputation for missing covariates was used to assess associations and potential vitamin C effect modification. Bayesian kernel machine regression was used to evaluate PFAS mixture associations. After adjustment for multiple comparisons, perfluorooctanoic acid (PFOA), perfluorohexane sulfonic acid (PFHxS), and perfluorodecanoic acid (PFDeA) were positively associated with bilirubin, and seven PFAS measures were positively associated with albumin. Albumin associations for PFOA, perfluorononanoic acid (PFNA), and PFDeA were stronger among vitamin C-deficient participants (q = 0.013). Mixture associations were positive for both biomarkers and consistent with the primary analysis. These findings suggest PFAS are associated with bilirubin and albumin; vitamin C findings are exploratory and limited by the small deficient group.

Background/Objectives: Identifying dietary factors influencing liver cancer is crucial for developing preventive measures. While tea polyphenols have demonstrated cancer-preventive activities in animal models, the evidence in humans is not definitive. This study aims to explore the association between tea consumption and liver cancer, as well as the interaction between tea drinking and other risk factors, in China, a country with a high incidence of liver cancer and substantial tea consumption. Methods: A population-based case–control study was conducted in Jiangsu Province from 2003 to 2010. Socio-demographic data, history of tea consumption, and serum markers of hepatitis B virus (HBV) and hepatitis C virus (HCV) infections were evaluated. Unconditional logistic regression was used to examine the associations between tea consumption and the odds of liver cancer. Potential interactions between tea consumption and other major liver cancer risk factors were assessed. Results: A total of 2011 incident liver cancer cases and 7933 controls were included in the analysis. Regular tea drinking showed an inverse association with the risk of liver cancer compared with those who never drank tea (OR: 0.79; 95% CI: 0.63–0.99). Current tea drinking showed an inverse association with liver cancer (OR: 0.51; 95% CI: 0.39–0.66), while former tea drinking showed a positive association (OR: 3.56; 95% CI: 2.42–5.23). Current tea consumption was inversely associated with liver cancer incidence among both hepatitis B surface antigen (HBsAg) positive (OR: 0.45; 95% CI: 0.28–0.73) and HBsAg negative participants (OR: 0.51, 95% CI: 0.36–0.73), among both never and ever tobacco smokers, ever alcohol drinkers (OR: 0.46; 95% CI: 0.33–0.63), and among those without family history of liver cancer. Multiplicative and additive interactions were observed between tea drinking and HBsAg, alcohol consumption, and history of raw water drinking. Conclusions: Tea consumption is inversely associated with the development of primary liver cancer, with potential interactions involving HBV infection, alcohol consumption, and raw (unsafe) water drinking. Increasing tea consumption—particularly among high-risk populations such as individuals who consume alcohol—may serve as an additional preventive measure for liver cancer. This should be considered alongside established strategies, including HBV vaccination, alcohol cessation, and avoidance of drinking raw water, to help reduce liver cancer risk.

Though indoor air pollution (IAP) is associated with elevated lung cancer risk, an integrated measure is imperative to thoroughly investigate this association. The interplay between sex and IAP on lung cancer remains unclear. We conducted a population‐based case‐control study in Jiangsu Province, China, from 2003 to 2010, with 2871 lung cancer cases and 8019 controls. Exposures and covariates information were collected via in‐person interviews using a standardized questionnaire. An integrated weighted risk score (WRS), accounting for the effect sizes of each source of IAP, was introduced. Unconditional logistic regression was employed to estimate adjusted odds ratios (aORs) and their 95% confidence intervals (CIs). Interactions between sex and IAP by tobacco smoking status were evaluated. Environmental tobacco smoking (ETS) (aOR = 1.54, 95% CI: 1.40, 1.69), poor ventilation (aOR = 1.18, 95% CI: 1.07, 1.30), and coal used for cooking (aOR = 1.27, 95% CI: 1.15, 1.41) were associated with lung cancer. Dose‐response relationships between lung cancer and WRS were observed, with p for trend less than 0.001. aOR for individuals at the highest quartile of the WRS of IAP was 1.74 (95% CI: 1.52, 2.00) compared to the lowest quartile. The associations were more profound among never‐smokers than ever‐smokers. Females tended to be more vulnerable to IAP, and sex interacted with IAP beyond multiplicativity on the odds scale. IAP is associated with lung cancer, with a stronger impact among never‐smokers. An interaction between IAP and sex was observed. These results underscore the importance of controlling IAP, especially ETS in order to reduce the risk of lung cancer.

Esophageal cancer continues to pose a significant public health issue in areas with increased incidence rates such as China. Although involuntary smoking was defined as a group 1 carcinogen for lung cancer, few studies have explored the impact of environmental tobacco smoking (ETS) on esophageal cancer. In this paper, we examined the association between ETS and esophageal cancer in high‐risk groups in Jiangsu Province, China. Epidemiologic data were collected for 2969 newly diagnosed cases and 8019 population controls including exposure to active/passive smoking and risk factors. The unconditional logistic regression model and the semi‐Bayes (SB) method were applied to assess adjusted odds ratios (ORs) and confidence intervals (CIs). ETS exposure (ever vs. never) was positively associated with esophageal cancer with an SB‐adjusted OR (95% CI) of 1.44 (1.31–1.58) among overall population, and 1.56 (1.35–1.82) among non‐smokers (i.e., non‐active smokers), with corresponding population attributable fractions of 15.0% (95% CI: 10.3%–18.9%) and 12.1% (95% CI: 8.8%–19.8%), respectively. The association was more prominent in men at work and in women at home, with SB‐adjusted OR (95% CI) of 1.36 (1.17–1.58) and 1.61 (1.35–1.58), respectively. A dose–response relationship between ETS exposure and the disease was detected across the entire population as well as in non‐smokers. This is the largest population‐based case–control study of ETS and esophageal cancer and the first study to evaluate such association among non‐smokers in a Chinese population. We recommend strengthening the ongoing anti‐tobacco public health initiatives in China with a particular emphasis on creating a tobacco‐free work/home environment.

BackgroundAlthough many studies suggested the benefit of smoking cessation among pregnant women in reducing the risk of preterm birth (PTB), the timing of the effect of the cessation remains inconclusive.ObjectivesTo examine the association of trimester-specific smoking cessation behaviours with PTB risk.MethodsWe included 199,453 live births in Western New York between 2004 and 2018. Based on self-reported cigarette smoking during preconception and in each trimester, we created six mutually exclusive groups: non-smokers, quitters in each trimester, those who smoked throughout pregnancy, and inconsistent smokers. Risk ratios (RRs) and 95% confidence intervals (CIs) were estimated using Poisson regression to examine the association between smoking cessation and PTB. Effect modification by illegal drug use, maternal age, race and ethnicity and pre-pregnancy body mass index (BMI) was investigated multiplicatively by ratio of relative risk and additively by relative excess risk due to interaction (RERI).ResultsOverall, 6.7% of women had a PTB; 14.1% smoked throughout pregnancy and 3.4%, 1.8% and 0.8% reported quitting smoking during the first, second and third trimesters, respectively. Compared to non-smokers, third-trimester cessation (RR 1.20, 95% CI 1.01, 1.43) and smoking throughout pregnancy (RR 1.27, 95% CI 1.21, 1.33) were associated with a higher PTB risk, while quitting smoking during the first or second trimester, or inconsistent smoking was not associated with PTB. A positive additive interaction was identified for maternal age and late smoking cessation or smoking throughout pregnancy on PTB risk (RERI 0.17, 95% CI 0.00, 0.36), and a negative interaction was observed for pre-pregnancy BMI >= 30 kg/m2 (ratio of relative risk 0.70, 95% CI 0.63, 0.78; RERI -0.42, 95% CI -0.56, -0.30).ConclusionCompared to non-smokers, smoking throughout pregnancy and third-trimester smoking cessation are associated with an increased risk of PTB, while quitting before the third trimester may not increase PTB risk.