Cause Of Lung Cancer Research Articles

Myths and Misconceptions Around Lung Cancer Causation in Palestine: Is It Time to Intervene?

Having an accurate knowledge of what truly increases the likelihood of developing lung cancer (LC) may help people make better decisions about lifestyle changes that could potentially lower their risk. This study assessed current beliefs in LC causation myths among Palestinians and explored factors associated with displaying good recognition of such myths. A national cross-sectional study was conducted from July 2019 to March 2020. A modified version of the Cancer Awareness Measure-Mythical Causes Scale was used for data collection. The awareness level of LC causation myths was determined based on the number of myths recognized to be incorrect: poor (0-4), fair (5-9), and good (10-13). A total of 4,817 participants completed the questionnaire of 5,174 approached (response rate = 93.1%). In total, 4,762 participants were included in the final analysis. Myths unrelated to food were more commonly recognized than food-related myths. The food-related myth most frequently recognized was eating burnt food (n = 1,427; 30.0%) followed by drinking from plastic bottles (n = 1,389; 29.2%). The food-related myth least commonly recognized was eating food containing additives (n = 737; 15.5%). The most frequently recognized myth unrelated to food was having a physical trauma (n = 2,903; 61%), whereas the least was using cleaning products (n = 1,140; 23.9%). Only 287 participants (6%) displayed good awareness. Having a chronic disease and knowing someone with cancer were associated with a decrease in the likelihood of displaying good awareness. Conversely, participants who were smoking cigarettes/shisha and those recruited from hospitals had an associated increase in the likelihood of displaying good awareness. This study found very poor awareness of LC causation myths, with only 6% recognizing ≥10 myths. Initiatives addressing LC mythical causes are needed.

Schweißrauchexpositionen in Deutschland und Bewertung der gesundheitsschädigenden Wirkungen – insbesondere im Hinblick auf Lungenkrebserkrankungen

Welding fume exposure in Germany and evaluation of the adverse effects on health, particularly in respect to lung cancer diseases Exposure to welding fumes can negatively affect human health in different ways. German legislation on occupational diseases (BKV) lists a variety of such diseases which can be recognised as occupational diseases in welders. Lung cancer is one of the diseases listed in the German legislation. In 2018, the International Agency for Research on Cancer (IARC) reevaluated the lung cancer risk of welders and, for the first time, found sufficient evidence for the causation of lung cancer. In Germany, therefore, discussions are currently under way on expanding the German list of recognised occupational diseases accordingly. This article contains information on various welding processes, the associated emission of welding fumes and the adverse health effects based on the IARC assessment, including the occupational diseases listed in the current German list of occupational diseases. Furthermore, an overview is given of the current status of exposure quantification and risk evaluation according to the literature as well as recommendations for the assessment of exposure to welding fumes. Keywords: welding fumes – occupational disease – lung cancer – risk evaluation

Study of clinical presentations of lung cancer in tertiary level hospital

Background: Lung cancer is the most common cancer diagnosed worldwide. It is also the leading contributor to cancer-related mortality, resulting in around 1.38 million cancer deaths per year worldwide. The aim and objective of the study was to study the clinical presentations including paraneoplastic manifestations and metastatic effects of lung cancer and to identify reasons for delay in diagnosis of lung cancer.Methods: Hospital based observational study was conducted on 100 consecutive cases.Results: Mean age of the cases with lung cancer was 56.36 years and 30% of the cases. Male predominance was seen with 63% males to 37% females. Tobacco smoking was present in 59% cases while exposure to second hand smoke and biomass fuel was seen in 11% and 9% patients. Most common presenting symptoms were cough (22.21%), chest pain (16.13%), fever (14.37%), dyspnea (11%) and hemoptysis (5.22%). Most common type of lung tumor was Adenocarcinoma (53%) followed by Small cell carcinoma (22%) and Squamous cell carcinoma (19%). Mutation analysis by molecular testing where possible in 76.66% NSCLC cases and showed with RAS (26.19%), EGFR (23.8%), ALK1 (11.9%) and ROS (4.7%) mutation. Stage I and II of lung cancer was seen in 17% cases while stage III and IV was seen in 39% and 44% cases respectively.Conclusions: Present study shown tobacco smoking as the most common risk factor in the causation of lung cancer (59%) followed by passive smoking (11%) and biomass fuel exposure (9%). Mortality in the present study was 72% in 2 years of follow up and Median survival in the study was 11 months. We recommend high index of suspicion in the high-risk groups as smokers and those with chronic respiratory diseases to avoid delay in diagnosis.

Is there a genomic fingerprint of Radon (Rn)-induced lung cancer (LC)? Comparison of genomic alterations in LC specimens from high and low Rn zones.

1572 Background: Rn-222 is a radioactive gas found in rocks and soil. It emits alpha particles that cause dsDNA breaks and increase potential for carcinogenesis. Rn is the 2nd leading cause of LC in the US after smoking. EPA estimates >15,000 deaths/yr (9% of LC deaths) from Rn. We hypothesize that the impact of Rn exposure may be reflected in LC gene mutation (mut) profiles. Methods: Using commercial NGS assays, we retrospectively analyzed genomic DNA alterations in FFPE specimens from 159 LC patients (pts) from the Lifespan Cancer Institute in Rhode Island (2014- 2019), followed by validation in a larger cohort of 5,532 pts using Caris platform. Based on EPA Rn maps, we identified counties with high indoor Rn levels (>4 pci/L; HR), and compared gene mut patterns with those from low Rn zones (<4 pci/L; LR). Based on pt’s zip code of residence, we categorized them to HR and LR. In the validation cohort, p values adjusted for multiple comparison (q) of < .05 were considered significant. Results: In the pilot cohort, 35 pts (22%) were in HR and 124 (78%) in LR zones. Adenocarcinoma histology was most frequent (73%) and smoking prevalence was high (75%) in both groups. Most prevalent alterations were TP53, KRAS and CDKN2A muts. In the HR, we noted more frequent recurrent muts in 2 DNA repair genes (DDR): ATM (11 vs 1%, p= .00086) and CHEK2 (6 vs 0%, p= .047) when compared to LR group. When classified into major pathways implicated in lung carcinogenesis, higher frequency of mutations were seen in DDR in HR zones vs. LR (29 vs 13%, p= .038). In the validation cohort, 1,433 (26%) pts were in HR and 4099 (74%) in LR zones. Among the DDR genes, ATM muts in HR group tended to be more frequent (4.7 vs 3.4% in LR, p= .03) as well as PALB2 (0.9 vs 0.4%, p= .02) while no difference seen in CHEK2. Other genes with significantly higher prevalence in HR were TP53, SMARCA4 and NFE2L2 (q< .05); while KMT2D, KEAP1, CDKN2A, MET, NF2, DNMT3A, CCND1 and FAS show a trend (p< .05). EGFR muts were significantly more frequent in LR zones (8.4 vs 14.6%, q= .001). Similar to the pilot cohort, DDR pathway alterations trend to be higher in HR zones (14 vs 12%, p= .05). Using a high TMB cut-off >10, tumors from HR zones had significantly higher TMB when compared to LR zones (56 vs 48%, q= .0005). Conclusions: To our knowledge, this is the first attempt to elucidate the pathobiology of Rn induced LC using gene mut analyses. Our observations suggest that LC associated with higher Rn exposure may have disabled DNA repair pathways and higher TMB. Assuming uniform tobacco smoke exposure, higher Rn was not associated with EGFR mut.

Asbestos, Smoking and Lung Cancer: An Update

This review updates the scientific literature concerning asbestos and lung cancer, emphasizing cumulative exposure and synergism between asbestos exposure and tobacco smoke, and proposes an evidence-based and equitable approach to compensation for asbestos-related lung cancer cases. This update is based on several earlier reviews written by the second and third authors on asbestos and lung cancer since 1995. We reevaluated the peer-reviewed epidemiologic studies. In addition, selected in vivo and in vitro animal studies and molecular and cellular studies in humans were included. We conclude that the mechanism of lung cancer causation induced by the interdependent coaction of asbestos fibers and tobacco smoke at a biological level is a multistage stochastic process with both agents acting conjointly at all times. The new knowledge gained through this review provides the evidence for synergism between asbestos exposure and tobacco smoke in lung cancer causation at a biological level. The evaluated statistical data conform best to a multiplicative model for the interaction effects of asbestos and smoking on the lung cancer risk, with no requirement for asbestosis. Any asbestos exposure, even in a heavy smoker, contributes to causation. Based on this information, we propose criteria for the attribution of lung cancer to asbestos in smokers and non-smokers.

Clinicopathological profile of primary lung cancer in a tertiary care teaching hospital in the south-east coast of India

Introduction: Lung is one of the commonest sites for neoplasms both primary and metastatic cancers. Identification and determination of histopathological play a major role in the diagnosis and treatment of cancer. Radiology and imaging helps in the selection of procedures to obtain a tissue sample for the diagnosis and management of lung cancer. The present study was aimed to analyze the clinic-pathological profile of primary lung cancer in the south-east coast of India. Materials and Methods: A prospective, observational study was conducted in the Department of Pulmonary Medicine, Maharaja Institute of Medical Sciences (MIMS), Vizianagaram, Andhra Pradesh, India. A total of 104 patients with primary lung cancer were enrolled. Radiological, clinico pathological profile and Histopathological analysis was done individually for all patients. Results: Male patients (70.1%) were more compared to females (29.9%). The Average age of the study population was 57.8 years. A total of 70(67.3%) study subjects had a history of smoking comprising of 61 males and 9 female subjects. Almost all study patients had clinical presentations of cough and shortness of breath (100%). Most common X-ray and CT chest radiographic feature was mass lesion (n=89 and n=91). Adenocarcinoma was identified in 79 patients (76.0%) as the most common histological type and it was also common in both smokers (n=49) and nonsmokers (n=29). Conclusions: The most common histological variant was Adenocarcinoma followed by squamous cell carcinoma. Among men, smoking is the principal risk factor in the causation of lung cancer. A precise, accurate and rapid screening method is still warranted for the diagnosis of primary lung cancer. Keywords: Adenocarcinoma, Bronchoscopy, Clinico-pathological profile, Histopathological profile, Primary lung cancer.

1845P - Tobacco use in lung cancer (LC) patients (p) in Spain

BackgroundTobacco use, mainly as cigarette smoking, is the leading cause of lung cancer. Eighty-five percent of LC occur in smokers. Understanding the Spanish smoking habits allows the government to design health care policies against this consumption. To do so, the Grupo Español de Cáncer de Pulmón (Spanish Lung Cancer Group) made this analysis within the context of the Thoracic Tumor Registry (TTR). MethodsThe TTR is an observational cohort multicenter study in Spain. The study is conducted according to the Declaration of Helsinki and approved by the institutional review board of each participating site. The registry was approved by the Spanish Drug Agency, as a non-post-authorization, non-interventional study. ResultsData have been collected from 6,600 LC from 58 different hospital sites across Spain. 12% (866 p) were non-smokers, 46% (3,039 p) were former smokers and 39% (2,611 p) were smokers. There were significant differences by gender, more women were non-smokers (37 % vs. 45% in males), meanwhile more former smokers were male (53.4% vs. 27.9% in women) (p-valor < 0.001). Significant differences were also observed in the study on the distribution of the smoking habit by year of diagnosis. In the last two years, the percentage of active smokers increased, both for the total population, as well as, for each one of the two genders separately. The increase was greater among the women and, also, the number of women who are active smokers is greater in recent years. Mean age of onset of the smoking habit was 18.2 years. Mean initiation age was less for men, 17.9 years in the men (95%CI 17.6-18.2 years) and 19.2 years in the women (95%CI 18.5-19.8 years) (p-valor < 0.001). Finally, it was found significant differences between Regional Communities in the mean age at onset of the habit, with much lower levels in the Valencian Community (16.6 years) or Navarra (16.9 years) regarding other regions, such as Murcia (22.9 years) or the Balearic Islands (21.6 years). ConclusionsTobacco use is the leading cause of LC in Spain accounting 85% of the cases. Consumption has increased in both genders, but specially in women, in our country among lung cancer patients. Tobacco cessation campaigns, especially in women, should be a priority in western countries, like Spain, and it has to be adapted to regional differences in tobacco use. Clinical trial identificationNCT02941458. Legal entity responsible for the studySpanish Lung Cancer Group. FundingNovartis, MSD, Lilly. DisclosureM. Provencio: Advisory / Consultancy: BMS; Advisory / Consultancy, Travel / Accommodation / Expenses: MSD; Advisory / Consultancy, Travel / Accommodation / Expenses: AstraZeneca; Advisory / Consultancy: Boehringer Ingelheim. All other authors have declared no conflicts of interest.

Lung cancer and family-centered concerns

Genetic and environmental interactions predispose certain groups to lung cancer, including families. Families or caregiving units experience the disease interdependently. We have previously evaluated the concerns and preferences of patients in addressing the lung cancer experience and cancer risks in their families. This qualitative study evaluates the concerns and preferences of family members and caregivers of patients with lung cancer in the lung cancer experience and familial cancer risks. We held focus groups to discuss the format and timing of addressing these preferences and concerns. Qualitative data generated was analyzed using a grounded theory approach. Five focus groups totaling 19 participants were conducted. Seven themes were identified: (1) journey to lung cancer diagnosis has core dimensions for patient and family, (2) importance of communication between patients, families, and providers, (3) challenges for caregivers and family, (4) mixed perceptions of lung cancer causation among relatives, (5) discussion of cancer risk with relatives has complex dynamics, (6) impact of diagnosis on family health behaviors and screening, (7) role of genetic counseling. Family members of patients with lung cancer are interested in discussing risk factors, prevention, and diagnoses and also would like access to other supportive services do learn about and cope with some of the stresses and barriers they experience in the family lung cancer journey. The diagnosis represents a potential teachable moment with the opportunity to reduce the risk of LC development or improve early detection in LC patient's family members.

Estimating the burden of lung cancer and the efficiency of home radon mitigation systems in some Canadian provinces

Lung cancer (LC) is the leading cause of death of cancer in Canada in both men and women, and indoor radon is the second leading cause of LC after tobacco smoking. The Population Attributable Risk (PAR) is used to assess radon exposure risk. In this work we estimate the burden of LC in some Canadian provinces. We use the PAR to identify the radon levels responsible for most LC cases. Finally, we use the PAR function of the two variables, radon action and target levels, to search for a possible optimal mitigation program. MethodsThe LC burden for Ontario, Alberta, Manitoba, Quebec and British Columbia was estimated using provincial radon and mortality data. Then the PAR and LC cases for these provinces were estimated over the period 2006–2009 at different given indoor radon exposure levels. Finally, the PAR function when radon action levels and radon target levels are variables was analyzed. ResultsThe highest burden of LC in 2006–2009 was in Ontario and Quebec. During the period 2006–2009, 6% of houses in Ontario, 9% of houses in Alberta, 19% of houses in Manitoba, 7% of houses in Quebec, and 5% of houses in British Columbia had radon levels higher than 200 Bq/m3 and were responsible about 913, 211, 260, 972, and 258 lives, respectively. Radon mitigation programs could have prevented these LC cases. The BEIR VI assumption for the United States (US) population, 95% of LC deaths in men and 90% of LC deaths in women are Ever-Smokers (ES), can be applied to the Canadian population. The PAR is a linear function in the target radon value with an estimated slope of 0.0001 for Ontario, Alberta, Quebec and British Columbia, and 0.0004 for Manitoba. The PAR is almost a square root function in the radon action level. The PAR is sensitive to changes in the radon mitigation program and as such, any improvement is a worthwhile investment.

PUB087 Domestic Cooking Fuel as a Risk Factor for Lung Cancer in Women - A Case Control Study

Tobacco smoking is the most common risk factor for lung cancer. But a significant proportion of lung cancer occurs in non-smokers. Indoor pollution due to domestic fuels has been recently implicated as a causative agent in lung cancer especially in women. We conducted a case control study to find out the role of Domestic Cooking Fuel as a risk factor for Lung Cancer in Indian women. In a case control study 67 women with proven lung cancer were recruited. Forty-six females having a non-malignant respiratory disease constituted the control group. The patients and controls were asked about the exposure in various cooking fuels using a questionnaire. There were 50 (74.6%) non-smokers and 17 (25.4%) smokers among the female cancer cases (p=0.016). Adenocarcinoma was the commonest histological type of malignancy (n=26, 38.8%) in the whole group and was the predominant form in the non-smoking females. Tobacco smoking was the most important risk factor for lung cancer with OR of 4.87 (95% CI 1.34-17.76). Among non-smokers out of all the cooking fuels the risk of development of lung cancer was highest for biomass fuel exposure with an odds ratio of 5.33 (95% CI 1.7-16.7).Use of mixed fuels was associated with a lesser risk (OR= 3.04, 95% CI 1.1-8.38). This study indicated that domestic cooking fuel exposure is an important risk factor in the causation of lung cancer among women in addition of exposure to tobacco smoke.

Mortality effects assessment of ambient PM2.5 pollution in the 74 leading cities of China

BackgroundAmbient fine particulate matter (PM2.5) pollution is currently a most severe and worrisome environmental problem in China. However, current knowledge of the health effects of this pollution is insufficient. ObjectivesThis study aims to provide an overall understanding regarding the long-term mortality effects of current PM2.5 pollution in China and the potential health benefits of realizing the goals stipulated in the ongoing action plan of Air Pollution Prevention and Control (APPC) and the targets suggested by the WHO. MethodsThree typical causes and all-cause of PM2.5-related mortality were considered. The log-linear exposure-response function was adopted, and a meta-analysis was used to determine the exposure-response coefficients, based on newly available data in China and abroad. ResultsIn the 74 leading cities of China, approximately 32% of the reported deaths, with a mortality rate of 1.9‰, were associated with PM2.5 in 2013, in which deaths from cardiovascular, respiratory and lung-cancer causes accounted for 20% of the reported deaths, with a mortality rate of 1.2‰. The regional difference is remarkable for the mortalities and proportions of the different causes. If the PM2.5 concentration goals of the APPC plan, the first interim and the guideline targets of the WHO could be achieved, the PM2.5-related all-cause mortality would be reduced by 25%, 64% and 95%, respectively, compared with that of 2013. ConclusionsPM2.5 pollution in China has incurred great health risks that are even worse than those of tobacco smoking. The health benefits of the APPC plan could be outstanding, although there is still great potential to improve future air quality.

Lung cancer in the Indian subcontinent.

Smoking tobacco, both cigarettes and beedis, is the principal risk factor for causation of lung cancer in Indian men; however, among Indian women, the association with smoking is not strong, suggesting that there could be other risk factors besides smoking. Despite numerous advances in recent years in terms of diagnostic methods, molecular changes, and therapeutic interventions, the outcomes of the lung cancer patients remain poor; hence, a better understanding of the risk factors may impact the preventive measures to be implemented at the community level. There is a lack of comprehensive data on lung cancer in India. In this review, we attempt to collate the available data on lung cancer from India.

38P Overall survival in non-smokers and quitters compared to smokers who develop lung cancer: Case–control data from routine clinical practice

recently implicated as a causative agent in lung cancer especially in women. We conducted a case control study to find out the role of Domestic Cooking Fuel as a risk factor for Lung Cancer in Indian women. Methods: In the case control study 67 women with proven lung cancer were recruited. Forty-six females having a non-malignant respiratory disease constituted the control group. The patients and controls were asked about the exposure in various cooking fuels using a questionnaire. Results: There were 50(74.6%) non-smokers and 17(25.4%) smokers among the female cancer cases (p = 0.016). Adenocarcinoma was the commonest histological type of malignancy (n = 26, 38.8%) in the whole group and was the predominant form in the non-smoking females. Tobacco smoking was the most important risk factor for lung cancer with OR of 4.87 (95% CI 1.34–17.76). Among non-smokers out of all the cooking fuels the risk of development of lung cancer was highest for biomass fuel exposure with an odds ratio of 5.33 (95% CI 1.7–16.7). Use of mixed fuels was associated with a lesser risk (OR=3.04, 95% CI 1.1–8.38). Conclusions: This study indicated that domestic cooking fuel exposure is an important risk factor in the causation of lung cancer among women in addition of exposure to tobacco smoke. Legal entity responsible for the study: PSM Dental College and Hospital Funding: PSM Dental College and Hospital Disclosure: All authors have declared no conflicts of interest.

The Associations of Selected Lifestyle Patterns and Lung Cancer Risk: An Evidence-based Update

Diagnosis of lung cancer (LC) has been fraught with difficulty and by the time of definitive diagnosis, most patients are in later stages of the disease. Epidemiological studies have demonstrated that lifestyle behaviors play an etiological role in LC risk; however data in the literature on this topic often appears inconclusive or require further study. Understanding of the mechanisms operating between lifestyle patterns and their impact on LC is important for the disease’s prevention and treatment. The purpose of this study was to review the current evidence on the role of diet, body mass index (BMI), physical activity, smoking, alcohol consumption, and sex hormone use in LC development based on meta-analyses, systematic reviews and previously published epidemiologic studies. Regarded as the foremost cause of LC, evidence from studies have indicated that tobacco smoking causes LC. Additionally, exposure to outdoor air pollution and/or occupational-related exposures increase LC risk. Further, frequent consumption of red meat, processed meat increases adenocarcinoma and squamous cell carcinoma. Inverse associations between the disease risk and BMI ≥25 kg/m2, higher level of physical activity, and fruit and vegetable consumption with a high frequency were reported. Future studies are warranted to validate the association between histologic subtypes of LC and lifestyle patterns.

Analysis of the levels of psychological distress and its influence factors in patients with lung cancer

Objective To understand the levels of psychological distress in patients with lung cancer, and analyze the reason and influential factors. Methods The general information of the patients and the distress thermometer (DT)were used to carry out the cross-sectional study in 117 patients with lung cancer received treatments from September 2013 to January 2014. Results The score of psychological distress in patients with lung cancer was (3.10±1.70) points, and 56 patients (47.9%)had the significant psychological distress (DT score≥4 points). The main cause of lung cancer psychological distress ranking in the top 10, in turn, was fear, pain, fatigue, sleep problems, fear, tension, economic problems, eating, breathing, constipation. Mutiple linear regression analysis showed that the number of chemotherapy, age, vocation could affect the total score of distress. Conclusions The patients with lung cancer have obvious psychological distress. Emotional and physical problems of the patients are the main reason of psychological distress of patients with lung cancer.The number of chemotherapy, age, vocation of the patients are related to the psychological distress of patients with lung cancer. Key words: Lung neoplasms; Psychological distress; Distress thermometer

Implications of Evolving Medical Science for Proof of Lung Cancer Causation

Summary Causal determination in cases of diseases involving multiple risk factors and long development time poses formidable challenges to judges and juries. Numerous scientific, medical and legal questions are involved. For example, is the mere presence of a factor known to be associated with elevated disease risk sufficient for a causal determination? If not, what level of exposure should be deemed sufficient, and how can that exposure be measured with adequate confidence over an extended period? In the presence of two or more factors associated with elevated disease risk, how can causation be demonstrated and apportioned among these factors, particularly when the potential effects of their interaction are unknown? With increasing knowledge of the molecular and genetic changes involved in disease development, what level of comprehension and proof is sufficient to implicate a specific risk factor in the complex causal mechanism of an individual’s disease? Lung cancer, notwithstanding its strong association with cigarette smoking, represents a group of diseases associated with both a variety of risk factors and relatively long development time. Both the published scientific literature and current clinical practice for the treatment of lung cancer, particularly lung adenocarcinoma, reflect the rapid changes that have occurred in this field over the past decade. These medical advances, in addition to promising better prognosis for some lung cancer patients, have implications for the proof of lung cancer causation in litigation in which plaintiffs contend that tobacco smoke exposure caused their disease. This is particularly true in cases arising in many European countries and other jurisdictions in which little or no histological or cytological information has been produced by plaintiffs. This paper examines the rapidly evolving science underpinning lung cancer diagnosis and treatment and its forensic implications. [Beitr. Tabakforsch. Int. 26 (2015) 298-311]

Historical Perspectives of the Causation of Lung Cancer

Lung cancer is the leading cause of cancer deaths worldwide. Less-known forces are involved in the etiology of lung cancer and have relevant implications for providers in ameliorating care. The purpose of this article is to discuss theories of causation of lung cancer using historical analyses of the evolution of the disease and incorporating related explanations integrating the relationships of science, nursing, medicine, and society. Literature from 160 years was searched and Thagard’s model of causation networks was used to exhibit how nursing and medicine were significant influences in lung cancer causation theory. Disease causation interfaces with sociological norms of behavior to form habits and rates of health behavior. Historically, nursing was detrimentally manipulated by the tobacco industry, engaging in harmful smoking behaviors, thus negatively affecting patient care. Understanding the underlying history behind lung cancer causation may empower nurses to play an active role in a patient’s health.

Study on the relations between smoking and the risk of age-specific lung cancer deaths in urban and rural areas of China

To study the association between smoking and lung cancer mortality of residents living in the urban and rural areas of China. Using the national census data on causes of death and case-control studies, stratified analysis was conducted by parameters as geography and age, to calculate the risk ratios, excess risks, average years lost for life expectancy by smoking in males and females in 103 cities/counties in China. Smoking increased the risks for lung cancer death in all ages older than 35 years of age, in urban and rural areas, through data analysis on 52 193 cases died from lung cancer in 1986 - 1988 and 307 934 matched controls in China. The risk ratio was 3.0 (95%CI: 2.9 - 3.1) with 53.0% excess for lung cancer deaths in the male smokers. The years lost for life expectancy were 18.5 in urban, and 17.7 in rural male smokers aged 35 to 69 years. Similarly, the risk ratio was 3.0 (95%CI: 2.9 - 3.1), with 26.0% excess for lung cancer deaths in female smokers. The life-expectancy lost was 13.0 and 20.4 for female smokers aged 35 to 69 years in urban and rural areas, respectively. In both urban and rural areas, risk on lung cancer deaths caused by smoking in all males and females aged at 35 years and older had been significantly increased. Control of smoking prevalence should play a vital role in the prevention of the lung cancer death risks in China.

Clinico-pathological profile of lung cancer in Uttarakhand.

Background:Lung cancer is one of the most aggressive and prevalent type of malignancy causing high morbidity and mortality. Tobacco smoking continues to be the leading cause of lung cancer worldwide. An increasing incidence of lung cancer has been observed in India.Objective:The aim of this study was to evaluate the clinico, a pathological profile of the lung cancer in hilly state of Uttrakhand.Materials and Methods:We performed a retrospective analysis of histopathologically proven cases of bronchogenic carcinoma admitted in our hospital from January 1998 to August 2005.Results:Our study included 203 patients with confirmed cases of lung cancer. Male to female ratio was 8.2:1. The common age group being 40-60 years, 9.86% of the patients were less than 40 years old age. Smoking was found to be the main risk factor in 81.77% patients. The most frequent symptom was cough (72.90%) followed by fever (58.12%). The most common radiological presentation was mess lesion (46.31%). The most common histopathological type was squamous cell carcinoma (SCC) (44.83%) followed by adenocarcinoma (19.78%) and small cell lung carcinoma (SCLC) (16.75%). The majority patients (73.29%) were diagnosed in the later stages of the disease (III B and IV).Conclusion:It was found out that SCC was the most frequent histopathological form. SCLC predominates below 40 year and SCC over 60 years of age. Smoking still remains the major risk factors in pathogenesis of lung cancer.

Virginia Berridge (ed.), Making health policy: networks in research and policy after 1945, Clio Medica 75, The Wellcome Series in the History of Medicine, Amsterdam, Rodopi, 2005, pp. vi, 338, €75.00, $94.00 (hardback 90-420-1824-0).

Virginia Berridge opens her introductory chapter with the words: “ ‘Evidence-based policy’ has become a popular and a political mantra in the last decade. It seemed self-evident in the late-twentieth and early-twenty-first centuries; of course policy and practice should be based on the best available evidence, research or science.” She closes, however, by pointing out that there has not been a rational relationship between research and policy making in health: “policy framed evidence rather than the other way round” (pp. 5, 29). The collection of case studies in this volume provides abundant evidence to support this claim. All the authors work or have been members of the history group at the London School of Hygiene and Tropical Medicine. The breadth of interests of this group has been a major strength, because it has allowed it to explore in detail not only the diversity of influences that bear down on policy makers, but the problems and debates about the “evidence” that they are supposed to use. Luc Berlivet goes directly to the heart of the matter in his chapter ‘ “Association or causation?” The debate on the scientific status of risk factor epidemiology, 1947–c.1965’. He describes the rise of chronic disease epidemiology towards its current status as a dominant research technique in medicine, using as his example what the celebratory historians are right to describe as the classical pioneering paradigmatic study, the aetiological role of tobacco smoke in the causation of lung cancer. In spite of the strength of the association, the conclusion of a causal link reached by researchers like the statistician Bradford Hill and the physician Richard Doll was contested. Berlivet's account shows that the sceptics were defeated not only by the accumulation of more epidemiological evidence and by the identification of carcinogens in the smoke itself, but by the undermining of the standing of those opponents with tobacco company links by the questioning of their objectivity. So even if the acceptance that smoking caused cancer was a success for chronic disease epidemiology, its triumph was not achieved without difficulties. Other chapters describe and analyse its application to more complex problems. Betsy Thom discusses alcohol policy from 1950 to 2000; Mark Bufton looks at ‘British expert advice on diet and heart disease’; and the rather limited impact of science on the provision of renal dialysis and intensive care in the UK is described by Jennifer Stanton. Stuart Anderson concludes his examination of British hospital pharmacy policy from 1948 to 1974 by saying that the policy process “is very much determined by the wider social, economic and political climate in which it operates” (p. 213). Virginia Berridge in her account of smoking policy in the 1970s points out that climate setting from this time was much influenced by the media. Media management and policy determination and implementation have in recent years gone far past the point of disentanglement; Kelly Loughlin's chapters on ‘The changing role of press and public relations at the BMA, 1940s–80s’ and ‘Reporting science, health and medicine in the 1950s and the '60s’ demonstrate why. A theme running through many chapters is the decline in the influence of doctors on policy—and an increase in the converse. Sarah Mars in her study on drug misuse shows how guidelines—not evidence based—led to losses in clinical autonomy. It is right that when historians study the making of policy they should investigate the doings of expert advisory committees. The big strength of this book is that it considers other things as well. Read it to find out why the BMA is not only one of the most effective trade unions in the world, but is still seen by opinion-formers as a source of dispassionate and authoritative advice.