***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Introduction : The incidence of lung cancer in women living in China is among the highest in the world but it does not appear that tobacco smoking is a major risk factor for lung cancer . As tobacco smoking is highly prevalent in Chinese men , exposure to environmental tobacco smoke ( ETS ) may play an important role in the development of lung cancer in Chinese women who never smoked . We conducted the present investigation because previous studies did not account for dietary habits or indoor air pollution from Chinese-style cooking and they did not assess the effect of occupational exposure to ETS . Methods : A population -based , case – control study was conducted to evaluate the relationship between lung cancer and exposure to ETS  among nonsmoking women living in Shanghai , China . Five-hundred and four women diagnosed with incident , primary lung cancer between February 1992 and January 1994 were identified through the population -based Shanghai Cancer Registry . A control group of 601 nonsmoking women was selected r and omly from the Shanghai Residential Registry , and was approximately frequency-matched to the age distribution of the lung cancer cases . Information on lifetime domestic and occupational exposure to ETS was obtained through face-to-face interviews . Adjusted odds ratios ( OR ) and 95 % confidence intervals ( CI ) were estimated by unconditional logistic regression . Results : The OR for ever exposed to ETS from spouses was 1.1 ( 95 % CI : 0.8–1.5 ) , and the OR for ever exposed to ETS at work was 1.7 ( 95 % CI : 1.3–2.3 ) . Furthermore , the OR increased with increasing number of hours of daily exposure to ETS in the workplace and with increasing number of smoking co-workers . No associations were found for exposure to ETS during childhood . Conclusions : The main findings of the present study are that long-term occupational exposure to ETS , both alone or in combination with exposures at home , conferred an increased risk of lung cancer among women who never smoked . The inconsistency of the results regarding exposure to ETS at home and at work may have been due to lower exposures at home Objective : To investigate whether the  Irish smoking ban  has had an impact on secondh and smoke ( SHS ) exposures for hospitality workers . Design , setting , and participants : Before and after the smoking ban  a cohort of workers ( n = 35 ) from a sample of city hotels ( n = 15 ) were tested for saliva cotinine concentrations and completed question naires . Additionally , a r and om sample ( n = 20 ) of city centre bars stratified by size ( range 400–5000 square feet ) , were tested for air nicotine concentrations using passive sample rs before and after the ban . Main outcome measures : Salivary cotinine concentrations ( ng/ml ) , duration of self reported exposures to secondh and smoke , air nicotine ( μg/cubic metre ) . Results : Cotinine concentrations reduced by 69 % , from 1.6 ng/ml to 0.5 ng/ml median ( SD 1.29 ; p < 0.005 ) . Overall 74 % of subjects experienced decreases ( range 16–99 % ) , with 60 % showing a halving of exposure levels at follow up . Self reported exposure to SHS at work showed a significant reduction from a median 30 hours a week to zero ( p < 0.001 ) . There was an 83 % reduction in air nicotine concentrations from median 35.5 µg/m3 to 5.95 µg/m3 ( p < 0.001 ) . At baseline , three bars ( 16 % ) were below the 6.8 μg/m3 air nicotine significant risk level for lung cancer alone ; at follow up this increased to 10 ( 53 % ) . Conclusions : Passive smoking and associated risks were significantly reduced but not totally eliminated . Exposure to SHS is still possible for those working where smoking is still allowed and those working where smoke may migrate from outdoor areas . Further research is required to assess the true extent and magnitude of these exposures Background Profile regression is a Bayesian statistical approach design ed for investigating the joint effect of multiple risk factors . It reduces dimensionality by using as its main unit of inference the exposure profiles of the subjects that is , the sequence of covariate values that correspond to each subject . Objectives We applied profile regression to a case – control study of lung cancer in nonsmokers , nested within the European Prospect i ve Investigation into Cancer and Nutrition ( EPIC ) cohort , to estimate the combined effect of environmental carcinogens and to explore possible gene – environment interactions . Methods We tailored and extended the profile regression approach to the analysis of case – control studies , allowing for the analysis of ordinal data and the computation of posterior odds ratios . We compared and contrasted our results with those obtained using st and ard logistic regression and classification tree methods , including multifactor dimensionality reduction . Results Profile regression strengthened previous observations in other study population s on the role of air pollutants , particularly particulate matter ≤ 10 μm in aerodynamic diameter ( PM10 ) , in lung cancer for nonsmokers . Covariates including living on a main road , exposure to PM10 and nitrogen dioxide , and carrying out manual work characterized high-risk subject profiles . Such combinations of risk factors were consistent with a priori expectations . In contrast , other methods gave less interpretable results . Conclusions We conclude that profile regression is a powerful tool for identifying risk profiles that express the joint effect of etiologically relevant variables in multifactorial diseases Biomass is widely used for fuel in developing countries . Particles and gases of biomass burning may cause changes in the lung . In this prospect i ve study we investigated histopathological changes in the lungs of 42 non-smoking women [ mean age ( 59±10 ) years ] caused by biomass smoke . We valuated exposure to biomass smoke , case histories , and the fi ndings of physical examination , radiology , bronchoscopy , and lung histopathology . Mean exposure to biomass smoke was ( 28±9 ) hour-year ( 1 hour-year equals 365 hours of exposure per year with average exposure of 1 hour a day ) . The radiological fi ndings were mass ( 42 % ) , reticulonodular opacities ( 31 % ) , mediastinal lymphadenopathy ( 26 % ) , pleuro-parenchymal fi brotic b and ing ( 19 % ) , widening of the pulmonary artery ( 14 % ) , ground glass ( 11 % ) , mosaic perfusion ( 9 % ) , consolidation ( 9 % ) , segmental or subsegmental atelectasis ( 7 % ) , and bronchiectasis ( 7 % ) . The patients were diagnosed with lung cancer ( 35 % ) , interstitial lung disease ( 31 % ) , sarcoidosis ( 9 % ) , tuberculosis ( 9 % ) , chronic obstructive pulmonary disease ( 4 % ) , chronic bronchitis ( 9 % ) , and metastasis ( 4 % ) .  Bronchoscopy showed pilies , oedema , erythema , bronchus narrowing , endobronchial tumour , mucosal irregularity , increased vascularisation , blue-black anthracotic plaques , mucosal oedema , and purulent secretion . Transbronchial biopsies revealed neutrophil and lymphocyte leucocytes in the perivascular , peribronchiolar , and interalveolar septa , slightly enlarged connective tissue , thickening of the basal membrane , thickening of interalveolar septa , intimal and medial thickening of the vascular wall and vascular lumen narrowing , anthracosis between the cells and in the bronchiole epithelium . These fi ndings confi rm that biomass smoke has important toxic effects on the lung parenchyma , interstitium , and pulmonary vessels that may result in malignancies The aim of this study was to estimate the effect of exposure to  secondh and tobacco smoke  on the incidence of lung adenocarcinoma in situ/minimally invasive adenocarcinoma ( AIS/MIA ) . Data from seven case – control studies participating in the International Lung Cancer Consortium ( ILCCO ) were pooled , result ing in 625 cases of AIS/MIA and 7,403 controls , of whom 170 cases and 3,035 controls were never smokers . Unconditional logistic regression was used to estimate adjusted ORs ( ORadj ) and 95 % confidence intervals ( CI ) , controlling for age , sex , race , smoking status ( ever/never ) , and pack-years of smoking . Study center was included in the models as a r and om-effects intercept term . Ever versus never exposure to secondh and tobacco smoke was positively associated with AIS/MIA incidence in all subjects ( ORadj = 1.48 ; 95 % CI , 1.14–1.93 ) and in never smokers ( ORadj = 1.45 ; 95 % CI , 1.00–2.12 ) . There was , however , appreciable heterogeneity of ORadj across studies ( P = 0.01 ) , and the pooled estimates were largely influenced by one large study ( 40 % of all cases and 30 % of all controls ) . These findings provide weak evidence for an effect of secondh and tobacco smoke exposure on AIS/MIA incidence . Further studies are needed to assess the impact of secondh and tobacco smoke exposure using the newly recommended classification of subtypes of lung adenocarcinoma . Cancer Epidemiol Biomarkers Prev ; 24(12 ) ; 1902–6 . © 2015 AACR Background : Several countries are discussing new legislation regarding the ban on smoking in public places , based on the growing evidence of the hazards of secondh and smoke ( SHS ) exposure . The objective of the present study is to quantitatively assess the relationship between smoking , SHS , and serum cotinine levels in the European Prospect i ve Investigation into Cancer and Nutrition ( EPIC ) cohort . Methods : From a study on lung cancer in the EPIC cohort , question naire information on smoking was collected at enrolment , and cotinine was measured in serum . Three statistical models were applied by using sample s available in a cross-section design : ( i ) cotinine levels by categories combining smoking and SHS ( n = 859 ) ; ( ii ) the effect of hours of passive smoking exposure in nonsmokers only ( n = 107 ) ; ( iii ) the effect of the number of cigarettes consumed per day in current smokers only ( n = 832 ) . All models were adjusted for country , sex , age , and body mass index . Results : Among nonsmokers , passive smokers presented significant differences in cotinine compared with nonexposed , with a marked ( but not significant ) difference among former-smokers . A one hour per day increment of SHS gave rise to a significant 2.58 nmol/L ( 0.45 ng/mL ) increase in mean serum cotinine ( P < 0.001 ) . In current smokers , a one cigarette per day increment gave rise to a significant 22.44 nmol/L ( 3.95 ng/mL ) increase in cotinine mean ( P < 0.001 ) . Conclusions : There is clear evidence that not only tobacco smoking but also involuntary exposure increases cotinine levels . Impact : This study strengthens the evidence for the benefits of a smoking ban in public places . Cancer Epidemiol Biomarkers Prev ; 20(5 ) ; 869–75 . © 2011 AACR Abstract Objectives To investigate the association between environmental tobacco smoke , plasma cotinine concentration , and respiratory cancer or death .  Design Nested case-control study within the European prospect i ve investigation into cancer and nutrition ( EPIC ) . Participants 303 020 people from the EPIC cohort ( total 500 000 ) who had never smoked or who had stopped smoking for at least 10 years , 123 479 of whom provided information on exposure to environmental tobacco smoke . Cases were people who developed respiratory cancers or died from respiratory conditions . Controls were matched for sex , age ( plus or minus 5 years ) , smoking status , country of recruitment , and time elapsed since recruitment . Main outcome measures Newly diagnosed cancer of lung , pharynx , and larynx ; deaths from chronic obstructive pulmonary disease or emphysema . Plasma cotinine concentration was measured in 1574 people . Results Over seven years of follow up , 97 people had newly diagnosed lung cancer , 20 had upper respiratory cancers ( pharynx , larynx ) , and 14 died from chronic obstructive pulmonary disease or emphysema . In the whole cohort exposure to environmental tobacco smoke was associated with increased risks ( hazard ratio 1.30 , 95 % confidence interval 0.87 to 1.95 , for all respiratory diseases ; 1.34 , 0.85 to 2.13 , for lung cancer alone ) . Higher results were found in the nested case-control study ( odds ratio 1.70 , 1.02 to 2.82 , for respiratory diseases ; 1.76 , 0.96 to 3.23 , for lung cancer alone ) . Odds ratios were consistently higher in former smokers than in those who had never smoked ; the association was limited to exposure related to work . Cotinine concentration was clearly associated with self reported exposure ( 3.30 , 2.07 to 5.23 , for detectable/non-detectable cotinine ) , but it was not associated with the risk of respiratory diseases or lung cancer . Frequent exposure to environmental tobacco smoke during childhood was associated with lung cancer in adulthood ( hazard ratio 3.63 , 1.19 to 11.11 , for daily exposure for many hours ) 
    Output:
    
Based on the results of this study , ETS might be an important risk factor of female lung cancer in non-smokers