Combined Effects of Lung Disease History, Environmental Exposures, and Family History of Lung Cancer to Susceptibility of Lung Cancer in Chinese Non-smokers

2021 ◽  
Author(s):  
Fanglin Yu ◽  
Rendong Xiao ◽  
Xu Li ◽  
Zhijian Hu ◽  
Lin Cai ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Family History ◽  
Environmental Factors ◽  
Lung Disease ◽  
Environmental Exposures ◽  
Collective Effects ◽  
Combined Effects ◽  
Cancer History ◽  
Increased Risk ◽  
History Of

Abstract Background: Although cigarette smoking is a major risk factor for lung cancer, the incidence rate of lung cancer among non-smokers is notable. The etiology and potential mechanism of non-smoker lung cancer are worthy of further research. This study was designed to explore the collective effects of environmental factors and the relationship between environmental exposure index (EEI) and lung cancer among non-smokers by evaluating the joint effects among lung disease history, environmental factors, and family history of lung cancer without smoking confounders.Methods: A total of 767 never-smoked lung cancer cases and 767 sex- and age-matched controls were selected from the department of Thoracic Surgery and Respiratory Medicine of three hospitals in Fujian, China. We used two methods to develop the EEI according to 12 statistically significant environmental risk factors. Restricted cubic spline (RCS) was applied to analyze the non-linear relationship between EEI and lung cancer in non-smokers. Combined effects, additive interaction, and multiplicative interaction were assessed among lung disease history, EEI, and family history of lung cancer to estimate susceptibility to develop lung cancer.Results: Lung disease history, especially asthma, was significantly associated with an increased risk of lung cancer with an odds ratio (OR) for asthma history of 14.720 (95% CI: 1.877–115.449). Family history of lung cancer was related to susceptibility of lung cancer (OR = 3.347, 95% CI: 1.930–5.806). According to type of relatives and cancer, a parental or children’s history and a sibling’s history of lung cancer were significantly associated with an increased risk of lung cancer. The positive association between EEI and lung cancer was apparently stronger in those with lung disease history or family lung cancer history. Furthermore, there was a addictive interaction between EEI and lung disease history, and a possibly addictive interaction between EEI and family lung cancer history on development of lung cancer.Conclusions: There were combined effects among lung disease history, environmental exposures, and family history of lung cancer toward susceptibility to lung cancer in Chinese non-smokers. Non-smokers who had a family history of lung cancer were at higher risk of lung cancer than non-smokers who had lung disease history. Non-smokers with family cancer history may obtain benefits from removal of environmental exposures and active treatment of lung disease.

scholarly journals Combined effects of lung disease history, environmental exposures, and family history of lung cancer to susceptibility of lung cancer in Chinese non-smokers

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Fanglin Yu ◽  
Rendong Xiao ◽  
Xu Li ◽  
Zhijian Hu ◽  
Lin Cai ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Family History ◽  
Environmental Factors ◽  
Lung Disease ◽  
Environmental Exposures ◽  
Collective Effects ◽  
Combined Effects ◽  
Cancer History ◽  
Increased Risk ◽  
History Of

Abstract Background Although cigarette smoking is a major risk factor for lung cancer, the incidence rate of lung cancer among non-smokers is notable. The etiology and potential mechanism of non-smoker lung cancer are worthy of further research. This study was designed to explore the collective effects of environmental factors and the relationship between environmental exposure index (EEI) and lung cancer among non-smokers by evaluating the joint effects among lung disease history, environmental factors, and family history of lung cancer without smoking confounders. Methods A total of 767 never-smoked lung cancer cases and 767 sex- and age-matched controls were selected from the department of Thoracic Surgery and Respiratory Medicine of three hospitals in Fujian, China. We used two methods to develop the EEI according to 12 statistically significant environmental risk factors. Restricted cubic spline (RCS) was applied to analyze the non-linear relationship between EEI and lung cancer in non-smokers. Combined effects, additive interaction, and multiplicative interaction were assessed among lung disease history, EEI, and family history of lung cancer to estimate susceptibility to develop lung cancer. Results Lung disease history, especially asthma, was significantly associated with an increased risk of lung cancer with an odds ratio (OR) for asthma history of 14.720 (95% CI: 1.877–115.449). Family history of lung cancer was related to susceptibility of lung cancer (OR = 3.347, 95% CI: 1.930–5.806). According to type of relatives and cancer, a parental or children’s history and a sibling’s history of lung cancer were significantly associated with an increased risk of lung cancer. The positive association between EEI and lung cancer was apparently stronger in those with lung disease history or family lung cancer history. Furthermore, there was a addictive interaction between EEI and lung disease history, and a possibly addictive interaction between EEI and family lung cancer history on development of lung cancer. Conclusions There were combined effects among lung disease history, environmental exposures, and family history of lung cancer toward susceptibility to lung cancer in Chinese non-smokers. Non-smokers who had a family history of lung cancer were at higher risk of lung cancer than non-smokers who had lung disease history. Non-smokers with family cancer history may obtain benefits from removal of environmental exposures and active treatment of lung disease.

scholarly journals Combined and interaction effect of Chlamydia pneumoniae infection and smoking on lung cancer: a case-control study in southeast China

2020 ◽  
Author(s):  
Xin Xu ◽  
Zhiqiang Liu ◽  
Weimin Xiong ◽  
Minglian Qiu ◽  
Shuling Kang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Environmental Factors ◽  
Passive Smoking ◽  
Chlamydia Pneumoniae ◽  
Case Control Study ◽  
Case Control ◽  
Combined Effects ◽  
History Of ◽  
Control Study ◽  
History Of Cancer

Abstract Objective: This case-control study investigated the role of Chlamydia pneumoniae (Cpn) infection in the pathogenesis of lung cancer and the combined and interaction effect of Chlamydia pneumoniae infection and smoking or other environmental factors.Methods: The study was comprised of 449 lung cancer patients and 512 age- and gender-matched healthy controls. All participants provided a 5-ml fasting peripheral venous blood sample for testing Cpn-specific IgG and IgA by using micro-immunofluorescence. Besides analyzing the associations between Cpn and lung cancer, combined effect analysis, logistic regression, and the excel table made by Andersson were used to analyze the combined and interaction effects of Cpn and environmental factors on lung cancer.Results: Compared to those with no evidence of serum Cpn IgA or Cpn IgG, those with both Cpn IgG+ and IgA+ had 2.00 times the risk (95% CI: 1.34 - 3.00) of developing lung cancer. Smokers with Cpn IgG+ or IgA+ were associated with a significantly increased risk of lung cancer, the adjusted OR was 1.79 (95% CI: 1.10-2.91) or 2.27(95% CI:1.38-3.72), respectively. Those exposed to passive smoking with Cpn IgG+ or IgA+ also increased the risk of lung cancer, the adjusted OR was 1.82 (95% CI: 1.20-2.77) or 1.87(95% CI:1.22-2.87), respectively. The similar results were also observed among alcohol drinking people. Multiplicative and additive interactions were not observed between Cpn infection and environmental factors. The combined effects of Cpn IgG+ or IgA+ and smoking, passive smoking, family history of cancer were found on lung cancer.Conclusion: The Cpn infection was potentially associated with primary lung cancer in the Chinese Han population and had combined effects with smoking, passive smoking, and the family history of cancer.

scholarly journals Combined and interaction effect of Chlamydia pneumoniae infection and smoking on lung cancer: a case-control study in southeast China

2020 ◽  
Author(s):  
Xin Xu ◽  
Zhiqiang Liu ◽  
Weimin Xiong ◽  
Minglian Qiu ◽  
Shuling Kang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Passive Smoking ◽  
Chlamydia Pneumoniae ◽  
Case Control Study ◽  
Case Control ◽  
Combined Effects ◽  
Increased Risk ◽  
History Of ◽  
Control Study ◽  
History Of Cancer

Abstract Background: This case-control study investigated the role of Chlamydia pneumoniae (Cpn) infection in the pathogenesis of lung cancer and the combined and interaction effect of Cpn infection, smoking, and various environmental factors.Methods: The study comprised 449 lung cancer patients and 512 age- and gender-matched healthy controls. All participants provided a 5 ml fasting peripheral venous blood sample for testing Cpn-specific IgG and IgA by using micro-immunofluorescence. Besides analyzing the associations between Cpn and lung cancer, combined effect analysis, logistic regression, and the Excel table made by Andersson were used to analyze the combined and interaction effects of Cpn and environmental factors on lung cancer.Results: Compared to those with no evidence of serum Cpn IgA or Cpn IgG, those with both Cpn IgG+ and IgA+ had 2.00 times the risk (95% CI: 1.34–3.00) of developing lung cancer. Cpn IgG+ or IgA+ was associated with a significantly increased risk of lung cancer among smokers; the adjusted odds ratio (OR) was 1.79 (95% CI: 1.10–2.91) and 2.27 (95% CI: 1.38–3.72), respectively. Those exposed to passive smoking with Cpn IgG+ or IgA+ also showed an increased risk of lung cancer; the adjusted OR was 1.82 (95% CI: 1.20–2.77) or 1.87 (95% CI: 1.22–2.87), respectively. Similar results were also observed among alcohol drinkers. Multiplicative and additive interactions were not observed between Cpn infection and environmental factors. The combined effects of Cpn IgG+ or IgA+ with smoking, passive smoking, and family history of cancer on lung cancer were determined.Conclusion: Cpn infection is potentially associated with primary lung cancer in the Chinese Han population and has combined effects with smoking, passive smoking, and family history of cancer.

scholarly journals Combined and interaction effect of chlamydia pneumoniae infection and smoking on lung cancer: a case-control study in Southeast China

BMC Cancer ◽  
2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Xin Xu ◽  
Zhiqiang Liu ◽  
Weimin Xiong ◽  
Minglian Qiu ◽  
Shuling Kang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Environmental Factors ◽  
Passive Smoking ◽  
Chlamydia Pneumoniae ◽  
Case Control Study ◽  
Case Control ◽  
Increased Risk ◽  
History Of ◽  
Control Study ◽  
History Of Cancer

Abstract Background This case-control study investigated the role of Chlamydia pneumoniae (Cpn) infection in the pathogenesis of lung cancer and the combined and interaction effect of Cpn infection, smoking, and various environmental factors. Methods The study comprised 449 lung cancer patients and 512 age- and sex-matched healthy controls. All participants provided a 5 ml fasting peripheral venous blood sample for testing Cpn-specific IgG and IgA by using micro-immunofluorescence. Besides analyzing the associations between Cpn and lung cancer, combined effect analysis, logistic regression, and the Excel table made by Andersson were used to analyze the combined and interaction effects of Cpn and environmental factors on lung cancer. Results Compared to those with no evidence of serum Cpn IgA or Cpn IgG, those with both Cpn IgG+ and IgA+ had 2.00 times the risk (95% CI: 1.34–3.00) of developing lung cancer. Cpn IgG+ or IgA+ was associated with a significantly increased risk of lung cancer among smokers; the adjusted odds ratio (OR) was 1.79 (95% CI: 1.10–2.91) and 2.27 (95% CI: 1.38–3.72), respectively. Those exposed to passive smoking with Cpn IgG+ or IgA+ also showed an increased risk of lung cancer; the adjusted OR was 1.82 (95% CI: 1.20–2.77) or 1.87 (95% CI: 1.22–2.87), respectively. Similar results were also observed among alcohol drinkers. Multiplicative and additive interactions were not observed between Cpn infection and environmental factors. The combined effects of Cpn IgG+ or IgA+ with smoking, passive smoking, and family history of cancer on lung cancer were determined. Conclusion Cpn infection is potentially associated with primary lung cancer in the Chinese Han population and has combined effects with smoking, passive smoking, and family history of cancer.

scholarly journals Increased risk of lung cancer in individuals with a family history of the disease: A pooled analysis from the International Lung Cancer Consortium

2012 ◽  
Vol 48 (13) ◽  
pp. 1957-1968 ◽  
Author(s):  
Michele L. Coté ◽  
Mei Liu ◽  
Stefano Bonassi ◽  
Monica Neri ◽  
Ann G. Schwartz ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Family History ◽  
Pooled Analysis ◽  
Increased Risk ◽  
History Of

scholarly journals Combined and interaction effect of Chlamydia pneumoniae infection and smoking on lung cancer: a case-control study in southeast China

2020 ◽  
Author(s):  
Xin Xu ◽  
Zhiqiang Liu ◽  
Weimin Xiong ◽  
Minglian Qiu ◽  
Shuling Kang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Environmental Factors ◽  
Passive Smoking ◽  
Chlamydia Pneumoniae ◽  
Case Control Study ◽  
Case Control ◽  
Combined Effects ◽  
History Of ◽  
Control Study ◽  
History Of Cancer

Abstract Background: This case-control study investigated the role of Chlamydia pneumoniae (Cpn) infection in the pathogenesis of lung cancer and the combined and interaction effect of Chlamydia pneumoniae infection and smoking or other environmental factors. Methods: The study was comprised of 449 lung cancer patients and 512 age- and gender-matched healthy controls. All participants provided a 5-ml fasting peripheral venous blood sample for testing Cpn-specific IgG and IgA by using micro-immunofluorescence. Besides analyzing the associations between Cpn and lung cancer, combined effect analysis, logistic regression, and the excel table made by Andersson were used to analyze the combined and interaction effects of Cpn and environmental factors on lung cancer. Results: Compared to those with no evidence of serum Cpn IgA or Cpn IgG, those with both Cpn IgG+ and IgA+ had 2.00 times the risk (95% CI: 1.34 - 3.00) of developing lung cancer. Smokers with Cpn IgG+ or IgA+ were associated with a significantly increased risk of lung cancer, the adjusted OR was 1.79 (95% CI: 1.10-2.91) or 2.27(95% CI:1.38-3.72), respectively. Those exposed to passive smoking with Cpn IgG+ or IgA+ also increased the risk of lung cancer, the adjusted OR was 1.82 (95% CI: 1.20-2.77) or 1.87(95% CI:1.22-2.87), respectively. The similar results were also observed among alcohol drinking people. Multiplicative and additive interactions were not observed between Cpn infection and environmental factors. The combined effects of Cpn IgG+ or IgA+ and smoking, passive smoking, family history of cancer were found on lung cancer. Conclusion: The Cpn infection was potentially associated with primary lung cancer in the Chinese Han population and had combined effects with smoking, passive smoking, and the family history of cancer. Keywords: Chlamydia pneumoniae infection, case-control study, environmental factors, lung cancer

scholarly journals Relationship between Air Pollution and Lung Cancer in Fujian Province: A Case-control study

2019 ◽  
Author(s):  
Guang-Min Chen ◽  
Fei He ◽  
Jiasheng Wu ◽  
Huimin Yang ◽  
Jin Su ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Air Pollution ◽  
Family History ◽  
Lung Disease ◽  
Medical History ◽  
Fruit Intake ◽  
Cooking Oil ◽  
Cooking Oil Fumes ◽  
History Of ◽  
Disease Family

Abstract Background: Outdoor air pollutants, especially particulate matters, are defined as a type of carcinogen by the International Agency for Research on Cancer. Studies have shown that air pollution is associated with lung cancer morbidity or mortality . This study is aimed at exploring the relationship between air pollutants and primary lung cancer in Fujian Province, China. Methods: We conducted a hospital-based, retrospective, case–control epidemiological study on three different populations to assess the occurrence of lung cancer caused by exposure to various levels of air pollution. Results: The total study population comprised 885 lung cancer patients and 1,220 healthy controls. The following parameters were identified as risk factors for lung cancer among the total population: smoking; exposure to cooking oil fumes; passive smoking; medical history of lung disease; family history of lung cancer; and exposure to PM10, PM2.5, and O3. Fruit intake and physical exercise were protective against lung cancer. For smokers, medical history of lung disease, family history of lung cancer, and exposure to PM10, and PM2.5 were risk factors for lung cancer, while fruit intake and physical exercise were protective factors. Among non-smokers, exposure to cooking oil fumes; medical history of lung disease; family history of lung cancer; and exposure to PM10, PM2.5, and O3 were factors increasing the risk of lung cancer, while fruit intake, physical exercise, and tea drinking were protective. Conclusions: Long-term exposure to PM10, PM2.5, and O3 was found to be significantly associated with increased risk of lung cancer, with the risk being greater for non-smokers and persons exposed to cooking oil fumes.

scholarly journals Relationship Between Air Pollution and Lung Cancer in Fujian Province: A Case-Control Study

2021 ◽  
Author(s):  
Guangmin Chen ◽  
Fei He ◽  
Jiasheng Wu ◽  
Huimin Yang ◽  
Jin Su ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Air Pollution ◽  
Family History ◽  
Lung Disease ◽  
Medical History ◽  
Fruit Intake ◽  
Cooking Oil ◽  
Cooking Oil Fumes ◽  
History Of ◽  
Disease Family

Abstract Background:Outdoor air pollutants, especially particulate matters, are defined as a type of carcinogen by the International Agency for Research on Cancer. Studies have shown that air pollutionis associated with lung cancer morbidity or mortality. This study is aimed at exploring the relationship between air pollutants and primary lung cancer in Fujian Province, China. Methods:We conducted a hospital-based, retrospective, case–control epidemiological study on three different populations to assess the occurrence of lung cancer caused by exposure to various levels of air pollution. Statistical analysiswas performed using the SPSS 25.0. Unconditional logistic regression modeling and identification of possible confounding factors were performed by calculating odds ratios (ORs) and 95% confidence intervals (CIs) for air pollution indexes and lung cancer risk. Results: The total study population comprised 885 lung cancer patients and 1,220 healthy controls. The following parameters were identified as risk factors for lung cancer among the total population: smoking; exposure to cooking oil fumes; passive smoking; medical history of lung disease; family history of lung cancer; and exposure to PM10, PM2.5, and O3. Fruit intake and physical exercise were protective against lung cancer. For smokers, medical history of lung disease, family history of lung cancer, and exposure to PM10, and PM2.5 were risk factors for lung cancer, while fruit intake and physical exercise were protective factors. Among non-smokers, exposure to cooking oil fumes; medical history of lung disease; family history of lung cancer; and exposure to PM10, PM2.5, and O3 were factors increasing the risk of lung cancer, while fruit intake, physical exercise, and tea drinking were protective factors. Conclusions: Long-term exposure to PM10, PM2.5, and O3 was found to be significantly associated with increased risk of lung cancer, with the risk being greater for non-smokers and persons exposed to cooking oil fumes.

Family History of Diabetes Is Associated with Increased Risk of Recurrent DKA in Pediatric Patients in Rhode Island

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1378-P
Author(s):  
JANAKI D. VAKHARIA ◽  
SUNGEETA AGRAWAL ◽  
JANINE BACIC ◽  
LISA S. TOPOR
Keyword(s):  
Family History ◽  
Rhode Island ◽  
Pediatric Patients ◽  
Family History Of Diabetes ◽  
Increased Risk ◽  
History Of

scholarly journals Vitamin D status and risk of type 2 diabetes in the Norwegian HUNT cohort study: does family history or genetic predisposition modify the association?

2021 ◽  
Vol 9 (1) ◽  
pp. e001948
Author(s):  
Marion Denos ◽  
Xiao-Mei Mai ◽  
Bjørn Olav Åsvold ◽  
Elin Pettersen Sørgjerd ◽  
Yue Chen ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Family History ◽  
Genetic Predisposition ◽  
Effect Modification ◽  
P Value ◽  
Family History Of Diabetes ◽  
Increased Risk ◽  
History Of

IntroductionWe sought to investigate the relationship between serum 25-hydroxyvitamin D (25(OH)D) level and the risk of type 2 diabetes mellitus (T2DM) in adults who participated in the Trøndelag Health Study (HUNT), and the possible effect modification by family history and genetic predisposition.Research design and methodsThis prospective study included 3574 diabetes-free adults at baseline who participated in the HUNT2 (1995–1997) and HUNT3 (2006–2008) surveys. Serum 25(OH)D levels were determined at baseline and classified as <50 and ≥50 nmol/L. Family history of diabetes was defined as self-reported diabetes among parents and siblings. A Polygenic Risk Score (PRS) for T2DM based on 166 single-nucleotide polymorphisms was generated. Incident T2DM was defined by self-report and/or non-fasting glucose levels greater than 11 mmol/L and serum glutamic acid decarboxylase antibody level of <0.08 antibody index at the follow-up. Multivariable logistic regression models were applied to calculate adjusted ORs with 95% CIs. Effect modification by family history or PRS was assessed by likelihood ratio test (LRT).ResultsOver 11 years of follow-up, 92 (2.6%) participants developed T2DM. A higher risk of incident T2DM was observed in participants with serum 25(OH)D level of<50 nmol/L compared with those of ≥50 nmol/L (OR 1.72, 95% CI 1.03 to 2.86). Level of 25(OH)D<50 nmol/L was associated with an increased risk of T2DM in adults without family history of diabetes (OR 3.87, 95% CI 1.62 to 9.24) but not in those with a family history (OR 0.72, 95% CI 0.32 to 1.62, p value for LRT=0.003). There was no effect modification by PRS (p value for LRT>0.23).ConclusionSerum 25(OH)D<50 nmol/L was associated with an increased risk of T2DM in Norwegian adults. The inverse association was modified by family history of diabetes but not by genetic predisposition to T2DM.

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