Risk Of Lung Cancer In Females Research Articles

Aristolochic Acid and the Risk of Female Lung Cancer: Population-Based Case-Control Study

Aristolochic Acid and the Risk of Female Lung Cancer: Population-Based Case-Control Study

Association of polycyclic aromatic hydrocarbons exposure scores and alteration of mitochondrial DNA copy number with female lung cancer risk among never smokers

To investigate the association of exposure to polycyclic aromatic hydrocarbons exposure scores and alteration of relative mitochondrial DNA copy number of blood with female lung cancer risk among never smokers. From August 2017 to August 2021, we enrolled all physician diagnosed new cases(n=465) of non-smoking female lung cancer from 12 tertiary and above hospitals in Liaoning, Jiangsu, Anhui and Qinghai provinces. And we selected matched non-smoking controls(n=463) by age and sex who were non-cancer and noncommunicable disease patients from the same hospital visited by the cases. Blood mitochondrial DNA copy number was detected by quantitative real-time polymerase chain reaction and estimated by relative quantification. We performed random forest and logistic regression to analyze the association of polycyclic aromatic hydrocarbons exposure scores and relative mitochondrial DNA copy number with the risk of female lung cancer among never smokers. We further analyzed the mediating effect and interaction models of polycyclic aromatic hydrocarbons exposure scores and mitochondrial DNA copy number levels on lung cancer in non-smoking women. The M(P25, P75) of polycyclic aromatic hydrocarbons exposure scores for cases and controls were 0.05(0.13, 0.16) and 0.08(0.24, 0.13), polycyclic aromatic hydrocarbons exposure scores of the cases was significantly higher than the controls(U=92130, P<0.05). The M(P25, P75) of mitochondrial DNA copy number for cases and controls were 0.90(0.71, 1.14) and 1.00(0.79, 1.21), mitochondrial DNA copy number of the cases was significantly lower than the controls(U=122559, P<0.05). Random forest and multivariable logistic regression analysis showed that the risk of lung cancer in non-smoking women increased with the increase of polycyclic aromatic hydrocarbons exposure scores(P_(trend)<0.05) and the decrease of relative mitochondrial DNA copy number(P_(trend)<0.05). The additive interaction between polycyclic aromatic hydrocarbons exposure scores and mitochondrial DNA copy number in non-smoking female lung cancer was statistically significant [API = 0.43(95%CI 0.19-0.67), SI = 2.84(95%CI 1.25-6.48). Mediation analysis showed mitochondrial DNA copy number had no significant mediating effect on the association between polycyclic aromatic hydrocarbons exposure scores and lung cancer in non-smoking women(Za×Zb: 95%CI-0.044-0.055). Minimize unnecessary polycyclic aromatic hydrocarbons exposures might significantly reduce the lung cancer risk among non-smoking women. Alteration of mitochondrial DNA copy number might become a potential biomarker in risk prediction of lung cancer of non-smoking women.

Bisphenol A and Di(2-Ethylhexyl) Phthalate promote pulmonary carcinoma in female rats via estrogen receptor beta: In vivo and in silico analysis

The prevalence of lung cancer in women currently merits our attentions. However, cigarette exposure alone does not tell the whole story that lung cancer is more prevalent among non-smoking women. Since female lung cancer is closely linked to estrogen levels, many of endocrine disrupting chemicals (EDCs), as the substances similar to estrogen, affect hormone levels and become a potential risk of female lung cancer. Additionally, the combined toxicity of EDCs in daily environment has only been discussed on a limited scale. Consequently, this study explored the cancer-promoting effect of two representative substances of EDCs namely Bisphenol A (BPA) and Di(2-Ethylhexyl) Phthalate (DEHP) after their exposure alone or in combination, using a rat pulmonary tumor model published previously, combining bioinformatics analysis based on The Comparative Toxicogenomics Database (CTD) and The Cancer Genome Atlas (TCGA) databases. It demonstrated that BPA and DEHP enhanced the promotion of pulmonary tumor in female rats, either alone or in combination. Mechanistically, BPA and DEHP mainly directly bound and activated ESR2 protein, phosphorylated CREB protein, activated HDAC6 transcriptionally, induced the production of the proto-oncogene c-MYC, and accelerated the formation of pulmonary tumor in female rats. Remarkably, BPA, rather than DEHP, exhibited a much more critical effect in female lung cancer. Additionally, the transcription factor ESR2 was most affected in carcinogenesis, causing genetic disruption. Furthermore, the TCGA database revealed that ESR2 could enhance the promotion and progression of non-small cell lung cancer in females via activating the WNT/β-catenin pathway. Finally, our findings demonstrated that BPA and DEHP could enhance the promotion of pulmonary carcinoma via ESR2 in female rats and provide a potential and valuable insight into the causes and prevention of lung cancer in non-smoking women due to EDCs exposure.

Flying without a Net: Space Radiation Cancer Risk Predictions without a Gamma-ray Basis.

The biological effects of high linear energy transfer (LET) radiation show both a qualitative and quantitative difference when compared to low-LET radiation. However, models used to estimate risks ignore qualitative differences and involve extensive use of gamma-ray data, including low-LET radiation epidemiology, quality factors (QF), and dose and dose-rate effectiveness factors (DDREF). We consider a risk prediction that avoids gamma-ray data by formulating a track structure model of excess relative risk (ERR) with parameters estimated from animal studies using high-LET radiation. The ERR model is applied with U.S. population cancer data to predict lifetime risks to astronauts. Results for male liver and female breast cancer risk show that the ERR model agrees fairly well with estimates of a QF model on non-targeted effects (NTE) and is about 2-fold higher than the QF model that ignores NTE. For male or female lung cancer risk, the ERR model predicts about a 3-fold and more than 7-fold lower risk compared to the QF models with or without NTE, respectively. We suggest a relative risk approach coupled with improved models of tissue-specific cancers should be pursued to reduce uncertainties in space radiation risk projections. This approach would avoid low-LET uncertainties, while including qualitive effects specific to high-LET radiation.

Associations between female lung cancer risk and sex steroid hormones: a systematic review and meta-analysis of the worldwide epidemiological evidence on endogenous and exogenous sex steroid hormones

BackgroundPublished findings suggest sex differences in lung cancer risk and a potential role for sex steroid hormones. Our aim was to perform a meta-analysis to investigate the effects of sex steroid hormone exposure specifically on the risk of lung cancer in women.MethodsThe PubMed, MEDLINE, Web of Science, and EMBASE databases were searched. The pooled odds ratios (ORs) and 95% confidence intervals (95% CIs) for female lung cancer risk associated with sex steroid hormones were calculated overall and by study design, publication year, population, and smoking status. Sensitivity analysis, publication bias, and subgroup analysis were performed.ResultsForty-eight studies published between 1987 and 2019 were included in the study with a total of 31,592 female lung cancer cases and 1,416,320 subjects without lung cancer. Overall, higher levels of sex steroid hormones, both endogenous (OR: 0.92, 95% CI: 0.87–0.98) and exogenous (OR: 0.86, 95% CI: 0.80–0.93), significantly decreased the risk of female lung cancer by 10% (OR: 0.90, 95% CI: 0.86–0.95). The risk of lung cancer decreased more significantly with a higher level of sex steroid hormones in non-smoking women (OR: 0.88, 95% CI: 0.78–0.99) than in smoking women (OR: 0.98, 95% CI: 0.77–1.03), especially in Asia women (OR: 0.84, 95% CI: 0.74–0.96).ConclusionsOur meta-analysis reveals an association between higher levels of sex steroid hormone exposure and the decreased risk of female lung cancer. Surveillance of sex steroid hormones might be used for identifying populations at high risk for lung cancer, especially among non-smoking women.

Association between sex hormones regulation-related SNP rs12233719 and lung cancer risk among never-smoking Chinese women.

BackgroundThe mechanism of rapidly increased non‐small cell lung cancer (NSCLC) among never‐smoking Chinese women has not been elucidated. Ovarian sex steroid hormones have been suggested to counteract lung cancer development, and sex hormone‐binding globulin (SHBG) is essential in sex hormones regulation. This study aims to exploring single nucleotide polymorphisms (SNPs) in genomic regions associated with SHBG concentrations that contributed to never‐smoking female NSCLC.MethodsCandidate genes were selected by a genome‐wide association (GWAS) meta‐analysis and gene expression profiles of never‐smoking NSCLC of Chinese women. The candidate SNPs limited to common minor allele frequency (MAF), missense variant, ethnic heterogeneous distribution, and SNPs were genotyped using the TaqMan method. A two‐stage case‐control design was adopted for exploration and validation of associations between candidate SNPs and risk of NSCLC. All participants were never‐smoking Chinese women. Chi‐square test and multivariate logistic regression were applied.ResultsBeginning with 12 genomic regions associated with circulating SHBG concentrations and gene expression profiles from never‐smoking NSCLC in Chinese women, candidate SNP rs12233719 and rs7439366 both located in candidate gene UGT2B7, which may be related to circulating SHBG concentrations and cancer risk, were identified. A two‐stage case‐control study was conducted in Shenyang and Tianjin represented as the training stage and validation stage, respectively. Under the dominant model, compared to individuals with the wild G/G genotype, the adjusted OR of those with the T allele was 1.58 (95% CI: 1.15–2.16) in Chinese Shenyang training set, and was 1.49 (95% CI: 1.02–2.18) in Chinese Tianjin validation set, both accompanied with a significant trend relationship consistently. UGT2B7 was upregulated in female NSCLC patients’ tumor tissues and was associated with a poor prognosis in NSCLC.ConclusionOur findings indicated that a sex hormones regulation‐related SNP rs12233719 was associated with never‐smoking female lung cancer risk, which might partially explain NSCLC‐susceptibility in Chinese women.

Meta-Analysis and Systematic Review in Environmental Tobacco Smoke Risk of Female Lung Cancer by Research Type.

More than 50% of women worldwide are exposed to Environmental Tobacco Smoke (ETS). The impact of ETS on lung cancer remains unclear. Cohort studies since the late 1990s have provided new evidence of female lung cancer risk due to ETS. The objective of this meta-analysis and systematic review was to analyze the association of ETS with female lung cancer risk from 1997 to 2017, organised based on research design. According to our applied inclusion and exclusion criteria, 41 published studies were included. The relative risk (RR) from the cohort studies or odds ratio (OR) from case-control studies were extracted to calculate the pooled risks based on the type of study. The summary risks of ETS were further explored with the modulators of ETS exposure sources and doses. The pooled risks of lung cancer in non-smoking women exposed to ETS were 1.35 (95% CI: 1.17–1.56), 1.17 (95% CI: 0.94–1.44), and 1.33 (95% CI: 1.17–1.51) for case-control studies, cohort studies, and both types of studies, respectively. The summary RR estimate of the cohort studies was not statistically significant, but the RR increased with increasing doses of ETS exposure (p trend < 0.05). Based on the results of this study, ETS might be an important risk factor of female lung cancer in non-smokers.

Correlation between use of simvastatin and lovastatin and female lung cancer risk: a nationwide case-control study.

The objective of this study was to determine the association between statin use and female lung cancer in Taiwan. In this case-control study, we used information from the Taiwan National Health Institute Research Database on 17,329 patients (cases) aged 20years or older recently diagnosed with lung cancer between 2005 and 2010 and 17,329 patients without lung cancer to assess the association between female lung cancer and statin use, even adjustment for its comorbidities. After adjusting for age and associated risk factors, we determined that women who engaged in long-term use of simvastatin at a defined daily dose (DDD) of over 150 have a reduced risk of lung cancer compared with those who did not use statins (odds ratio: 0.77, 95% confidence interval: 0.62-0.97) in women. However, lovastatin was not significantly associated with lung cancer in women. Among female patients with pre-existing comorbidities of respiratory diseases such as chronic obstructive pulmonary disease, hypertension, stroke and pulmonary tuberculosis, statins reduced the risk of lung cancer. Simvastatin use at a DDD of more than 150 is correlated with an approximately 20% reduction in the risk of lung cancer in women.

Abstract A46: Vitamin E intake and the lung cancer risk among female nonsmokers: A report from the Shanghai Women's Health Study

Abstract Background: Tocopherols, as the major source of vitamin E in diet in China and US, include four isoforms (α, β, γ, and δ) differentiated by the number and position of methyl groups on the chromanol ring. Tocopherols may inhibit carcinogenesis through inhibition of cell proliferation, induction of apoptosis, inhibition of angiogenesis, and enhancement of immune function. Results of past prospective studies and randomized controlled trials that evaluated the association between tocopherols intake and female lung cancer risk have been inconsistent and did not take into consideration lung cancer histology. Methods: We prospectively evaluated the association between tocopherol isoforms from diet, vitamin E supplement use, and lung cancer risk in 72,829 Chinese female nonsmokers aged 40-70 years and participating in the Shanghai Women's Health Study (SWHS). Tocopherol exposure from dietary and supplements sources were assessed through a validated food-frequency questionnaire at baseline and reassessed during follow-up. Cox proportional hazards models with time-dependent analysis were used to calculate multivariate-adjusted Hazard ratios (HRs) and 95% confidence interval (CIs) for lung cancer. All statistical tests were two sided. Results: Between January 1997 and December 2010, 481 study participants were diagnosed with lung cancer after study enrollment. Total dietary tocopherol was inversely associated with lung cancer risk among women complying with suggested dietary guidelines for adequate intake (AI) of tocopherol (14 mg/day or more: HR: 0.73; 95% CI = 0.54-0.99; compared to the lowest category) with a significant dose-response trend (P trend=0.045). Furthermore, borderline significant inverse associations were observed for combined dietary combined β and γ tocopherol (HR: 0.79; 95% CI = 0.59-1.06), and δ-tocopherols intake (HR: 0.78; 95% CI = 0.59-1.04). Additionally, there was a significant interaction effect between vitamin E or multivitamin supplements use and total dietary tocopherol intake in analysis using AI of tocopherol (P interaction = 0.018). In contrast, vitamin E supplement use was associated with a significant increase in lung cancer risk (HR: 1.39; 95% CI = 1.07-1.82). Analyses of lung cancer histology found that vitamin E supplement use was associated with increased risk of adenocarcinoma (HR: 1.79; 95% CI = 1.23-2.60). Exclusion of 45 cases diagnosed within two years of follow-up did not change the HR estimations appreciably. Conclusion: Total dietary tocopherol may be associated with lower lung cancer risk among female non-smokers, while tocopherol from vitamin supplements use was significantly associated with increased lung adenocarcinoma risk. Our results require confirmation in other prospective studies. Citation Format: Qi-Jun Wu, Yong-Bing Xiang, Gong Yang, Hong-Lan Li, Qing Lan, Yu-Tang Gao, Wei Zheng, Xiao-Ou Shu, Jay Fowke. Vitamin E intake and the lung cancer risk among female nonsmokers: A report from the Shanghai Women's Health Study. [abstract]. In: Proceedings of the Twelfth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2013 Oct 27-30; National Harbor, MD. Philadelphia (PA): AACR; Can Prev Res 2013;6(11 Suppl): Abstract nr A46.

Cruciferous vegetables consumption and the risk of female lung cancer: a prospective study and a meta-analysis

BackgroundEpidemiological studies evaluating the association between cruciferous vegetables (CVs) intake and female lung cancer risk have produced inconsistent results. Patients and methodsThis study followed 74 914 Chinese women aged 40–70 years who participated in the Shanghai Women's Health Study. CV intake was assessed through a validated food-frequency questionnaire (FFQ) at baseline and reassessed during follow-up. Hazard ratios (HRs) and 95% confidence interval (CIs) were estimated by using Cox proportional hazards models. Furthermore, we carried out a meta-analysis of all observational studies until December 2011. ResultsAfter excluding the first 2 years of follow-up, 417 women developed lung cancer over a mean of 11.1 years of follow-up. An inverse association of borderline statistical significance was observed between CV consumption and female lung cancer risk, with HR for the highest compared with the lowest quartiles of 0.73 (95% CI 0.54–1.00, P trend = 0.1607). The association was strengthened in analyses restricting to never smokers, with the corresponding HR of 0.59 (95% CI 0.40–0.87, P trend = 0.0510). The finding of an inverse association between CV intake and lung cancer risk in women was supported by our meta-analysis of 10 included studies. ConclusionsOur study suggests that CV consumption may reduce the risk of lung cancer in women, particularly among never smokers.

Statins use and female lung cancer risk in Taiwan

In11The first two authors contributed equally to this study. this present study, we found that the use of rosuvastatin with cumulative using duration >12 months could correlate with 2.8-fold increased risk of lung cancer in women. We did not have specific comments on these results. Further prospective clinical studies of statins use are needed to elucidate this issue.

CYP1A1 polymorphisms, lack of glutathione S-transferase M1 (GSTM1), cooking oil fumes and lung cancer risk in non-smoking women

to study the correlation of polymorphisms of CYP1A1 MspI, GSTM1 null genotype, cooking oil fumes independently and in combination with the risk of non-smoking lung cancer in females. one hundred and sixty female non-smoking patients with primary lung cancer and 160 controls were enrolled from Xiangya Hospital of Central South University. PCR-RELP and PCR were used to detect the distribution of CYP1A1 MspI and GSTM1 genotypes respectively. The correlation of these genes and cooking oil fumes with the susceptibility to lung cancer was analyzed. There was a significant difference in the frequencies of cooking oil fumes exposure between cancer cases and controls (χ(2) = 10.734, P < 0.01);but there was no statistical difference in CYP1A1 MspI polymorphisms between the 2 groups (χ(2) = 3.731, P > 0.05). The combination of CYP1A1 polymorphisms and cooking oil fumes significantly increased the risk of lung cancer. The frequencies of GSTM1 null genotype was significantly different between cancer cases and controls (χ(2) = 0.518, P < 0.05). The risk of lung cancer was higher in those with the GSTM1 null genotype and the OR was 1.697 (95%CI 1.090 - 2.640). Individuals with both GSTM1 null genotype and exposure to cooking fumes had a higher risk of cancer than those with only one of them, the OR being 3.617 (95%CI 1.899 - 6.891). The combination of the two genes significantly increased the risk of lung cancer. cooking oil fumes exposure was a risk factor for non-smoking lung cancer in females. The combination of CYP1A1 with cooking oil fume increased the risk of female lung cancer. GSTM1 null genotype was associated with risk of lung cancer in non-smoking females. The combination of GSTM1 null genotype and cooking oil fumes significantly increased the risk of female lung cancer. The combination of CYP1A1 and GSTM1 significantly increased the risk of lung cancer.

Ambient Exposure to Criteria Air Pollutants and Female Lung Cancer in Taiwan

To investigate the relationship between air pollution and female lung cancer, the authors conducted a matched case-control study using female deaths that occurred in Taiwan from 1995 through 2005. Data on all eligible female lung cancer deaths were obtained from the Bureau of Vital Statistics of the Taiwan Provincial Department of Health. The control group consisted of women who died from causes other than cancer or diseases associated with respiratory problems. The controls were pair-matched to the cases by sex, year of birth, and year of-death. Each matched control was selected randomly from the set of possible controls for each case. Classification of exposure to municipality air pollution was based on the measured levels of nitrogen dioxide and carbon monoxide. The results of the present study show that there is a significant positive association between the levels of air pollution and female lung cancer mortality. The adjusted odds ratios (95% confidence interval) were 1.24 (1.03–1.50) for the group with medium air pollution level and 1.46 (1.18–1.81) for the group with high air pollution level when compared to the group with the low air pollution level. Trend analyses showed statistically significant trend in risk of female lung cancer with increasing air pollution level. The findings of this study warrant further investigation of the role of air pollutants in the etiology of lung cancer.

Alcohol Drinking and Lung Cancer Risk: An Evaluation Based on a Systematic Review of Epidemiologic Evidence among the Japanese Population

The relationship between alcohol consumption and risk of lung cancer is controversial. Based on a systematic review of epidemiologic evidence, we evaluated this association among the Japanese population, who may be more susceptible to alcohol-related diseases than Western populations. Original data were obtained from MEDLINE searches using PubMed or from searches of the Ichushi database, complemented with manual searches. The evaluation of associations was based on the strength of evidence and the magnitude of association, together with biological plausibility as previously evaluated by the International Agency for Research on Cancer. We identified seven cohort studies and two case-control studies. One cohort study demonstrated a strong positive association between alcohol drinking and the risk of female lung cancer, but the association almost disappeared after adjustment for smoking. The other eight studies showed a weak positive or no association. Although smoking is the best-established risk factor for lung cancer, only five cohort studies presented smoking-adjusted risks out of all nine identified. Furthermore, only two studies explicitly reported the risk estimate for ex-drinkers who may have quit alcohol drinking after the development or diagnosis of the disease and have an apparently higher risk. We conclude that the epidemiologic evidence on the association between alcohol drinking and lung cancer risk remains insufficient in terms of both the number and methodological quality of studies among the Japanese population.

Women and lung cancer: does oestrogen play a role?

Smoking-related disease remains a major public-health problem. Large numbers of women continue to smoke, and new smokers are almost as likely to be female as male. Lung cancer is still a largely incurable disease; annual lung-cancer mortality in women exceeds that of breast cancer, and lung cancer now accounts for 12% of all new female cancer cases. The results of several studies suggest that women are more susceptible than men to lung cancer and to conditions that predispose to this cancer, such as chronic obstructive pulmonary disease. There is still much controversy about whether there is an increased lung-cancer risk in women across all populations. Many epidemiological studies have been negative or equivocal when comparing male and female lung-cancer risk. This article is not intended to be a comprehensive review of all epidemiological studies, or of all possible lung-cancer risk factors. Lung-cancer incidence and risk in women are discussed, and evidence for possible mechanisms of increased female risk are presented, including the role of oestrogen in the development of lung cancer.

Risk factors for lung cancer among women in Poland

A total of 118 women with histologically confirmed lung cancer and 141 healthy controls, were involved in a case-control study conducted in Cracow between 1991 and 1994. The aim of this study was to examine of the role of smoking, alcohol consumption, and diet in female lung cancer risk. Multivariate analysis has shown that cigarette smoking was the most strongly active risk factor in female lung cancer. Vodka drinkers showed significantly higher risk than non-drinking women. Frequent intakes of carrots (at least three times a week) significantly lowered the risk. The significant protective effect was also observed in women using margarine on bread. The analysis of dose-response relationship in reference to cigarette smoking, vodka drinking and consumption of carrots also confirmed significant influence of these factors on risk.

A case-control study of childhood and adolescent exposure to environmental tobacco smoke (ETS) and the risk of female lung cancer

A case-control study of childhood and adolescent exposure to environmental tobacco smoke (ETS) and the risk of female lung cancer

A case-control study of childhood and adolescent exposure to environmental tobacco smoke (ETS) and the risk of female lung cancer

A case-control study of childhood and adolescent exposure to environmental tobacco smoke (ETS) and the risk of female lung cancer

Childhood and adolescent passive smoking and the risk of female lung cancer.

Few studies have reported the relationship between passive smoking (PS) in early life and the risk of lung cancer. This study was done to evaluate the risk of female lung cancer from PS, especially that during childhood and adolescence. Using household exposure to tobacco smoke as an estimate of PS, a 1:1 paired case-control study was conducted in Harbin, China. We interviewed 114 female primary lung cancer cases, aged 30-69 years, and their hospital-based controls. The controls were non-cancer patients, selected from the same hospital as the cases, and matched on age (+/- 5 years), residential area and smoking status over their lifetime. There were 59 pairs who ever smoked and 55 pairs who never smoked. Information on PS was collected by residence for each of the following periods: 0-6, 7-14, 15-22, 23-30 and 31-69 years. Household PS significantly increases the risk of female lung cancer for those exposed at ages 22 or younger, who have ever smoked. The risk was also increased for those non-smoking pairs when exposed under the age of 15 years. Exposure to maternal smoking at ages 14 or younger increased the risk by about 170% (odds ratio, OR 2.7, 95% confidence interval [CI]: 1.49-4.88), but not to paternal smoking (OR 1.40, 95%CI: 0.92-2.50). The risk was highest for those exposed under the age of seven (OR 3.46, 95%CI: 1.80-6.65) and was also significant at ages 7-14 (OR 3.08, 95% CI: 1.62-5.57) and 15-22 (OR 3.10, 95%CI: 1.52-6.31) years. Under the age of 23 years, the OR increased with amount of PS (P < 0.001). Of note, the OR in all five exposure periods for non-smoking pairs were similar to those for all 114 pairs studied. Household PS, particularly that during childhood, increases the risk of female lung cancer. The assessment of PS should be done by different periods of exposure.