scholarly journals Methodological problems in epidemiological data: the case of correlation between radon level and lung cancer

2020 ◽  
Vol 11 (3/4) ◽  
pp. 207
Author(s):  
Joanna Reszczyńska ◽  
Maciej Pylak ◽  
Krzysztof W. Fornalski ◽  
S.J. Mortazavi ◽  
L. Dobrzyński
2020 ◽  
Vol 11 (3/4) ◽  
pp. 207
Author(s):  
S.J. Mortazavi ◽  
Maciej Pylak ◽  
Krzysztof W. Fornalski ◽  
L. Dobrzyński ◽  
Joanna Reszczyńska

2019 ◽  
Vol 76 (Suppl 1) ◽  
pp. A53.1-A53
Author(s):  
Mathilde Boulanger ◽  
Severine Tual ◽  
Romain Pons ◽  
Amandine Busson ◽  
Patricia Delafosse ◽  
...  

ContextExposure to inorganic arsenicals, including occupational use of pesticides, is carcinogenic to the lung (IARC group 1). However epidemiological data are scarce for agricultural exposures. This work assesses lung cancer (LC) risk, including duration-effect relationships, associated to arsenicals use in farming, by gender and histology.MethodsWe linked data from two French projects: (1) the Agriculture and Cancer (AGRICAN) cohort, a large prospective cohort of farmers and people affiliated to the French agricultural insurance scheme and (2) the Pesticide Matrix (PESTIMAT), a crop-exposure matrix. Incident lung cancer cases were collected and their histological subtype ascertained from cancer registries, from enrolment (2005–2007) to December 31 st 2013. The enrolment questionnaire included items on smoking history, and the involvement in 18 different breedings/crops and specific tasks, including pesticide application, with years of beginning and end. We performed Cox models, with age as timescale, adjusted on gender, smoking, and two activities found to be protective in previous analyses – cattle breeding and corn growing. The reference group included farmers having never applied any pesticide on any crop. We assessed risks for each inorganic compound (lead, sodium, aluminum, copper and calcium arsenate) and for overall exposure.ResultsNearly 10% (n=14 359 people) of the population was potentially exposed to arsenicals, in vineyard growing before 2001, or in fruit-tree or potato growing before 1973. We observed 98 incident LC among exposed people. Only women exhibited a higher risk of LC (HR 3.14 95% CI(1.42–6.96) for exposure to any compound, n=7 exposed cases, all adenocarcinomas), but with no duration-effect relationship. Risks were significantly elevated for lead, copper and sodium arsenate.ConclusionWe found an increased risk of LC, especially adenocarcinomas, among women. At this stage, exposure assessment was broad: the use of an exposure index, based on probability, frequency and intensity of use, will help refine the analyses.


Author(s):  
Ole J. Benedictow

This article addresses the recent use of mathematical epidemiological SIR or SEIR models in plague research. This use of S(E)IR models is highly problematic, but the problems are not presented and considered. Serious problems show in that such models are used to “prove” that historical plague was a (1) Filoviridae disease and (2) a bacterial disease caused by Yersinia pestis which was transmitted by human fleas and lice. (3) They also support early-phase transmission (by fleas). They purportedly consistently disprove (4) the conventional view that plague is/was a rat-and-rat-flea-borne disease. For these reasons, the focus is on methodological problems and on empirical testing by modern medical, entomological, and historical epidemiological data. An important or predominant vectorial role in plague epidemics for human fleas and lice requires that several necessary conditions are satisfied, which are generally not considered by advocates of the human ectoparasite hypothesis of plague transmission: (1) the prevalence and levels of human plague bacteraemia (human plague cases as sources of infection of feeding human ectoparasites); (2) the general size of blood meals ingested by human fleas and lice; (3) the consequent number of ingested plague bacteria; (4) the lethal dose of bacteria for 50% of a normal sample of infected human beings, LD50; and (5) efficient mechanism of transmission by lice and by fleas. The factual answers to these crucial questions can be ascertained and shown to invalidate the human ectoparasite hypothesis. The view of the standard works on plague has been corroborated, that bubonic plague, historical and modern, is/was a rat-and-rat-flea-borne disease caused by Yersinia pestis. These conclusions are concordant with and corroborate recent studies which, by laboratory experiments, invalidated the early-transmission hypothesis as a mechanism of transmission of LDs to humans in plague epidemics and removed this solution to the problem of transmission by human fleas.


2018 ◽  
Vol 39 (7) ◽  
pp. 948-954 ◽  
Author(s):  
Jian-Min Yuan ◽  
Steven G Carmella ◽  
Renwei Wang ◽  
Yu-Ting Tan ◽  
Jennifer Adams-Haduch ◽  
...  

Abstract It has been hypothesized that the pathogenesis of lung cancer induced by cigarette smoking involves oxidative damage by free radicals. Epidemiological data on biomarkers of oxidative damage and risk of lung cancer development are sparse. A nested case–control study of 610 lung cancer cases and 610 matched controls was conducted within a prospective cohort of 18 244 Chinese men in Shanghai, China. The concentrations of 8-epi-prostaglandin F2α (8-epiPGF2α), a biomarker of oxidative stress, were determined in baseline urine samples using a validated mass-spectrometry assay. Current smokers had significantly higher level of 8-epiPGF2α than former smokers or never smokers (P < 0.001). 8-epiPGF2α levels were significantly higher in lung cancer cases than their smoking-matched controls in former and current smokers, but not different in never smokers (P for interaction = 0.019). The relative risks of developing lung cancer for former and current smokers in the highest relative to the lowest quartile of 8-epiPGF2α were 5.25 (Ptrend = 0.035) and 1.99 (Ptrend =0.007), respectively. The effect of 8-epiPGF2α and biomarkers of cigarette smoke exposure on lung cancer risk was additive; the relative risk was 5.33 (95% confidence interval = 2.65–7.51) for current smokers with the highest thirds of 8-epiPGF2α and total cotinine compared with their lowest thirds. Smokers with a heightened state of oxidative stress in response to the insults of cigarette smoking may be more susceptible to smoking-induced lung carcinogenesis.


2017 ◽  
Vol 49 (4) ◽  
pp. 1601734 ◽  
Author(s):  
Olivier Calvayrac ◽  
Anne Pradines ◽  
Elvire Pons ◽  
Julien Mazières ◽  
Nicolas Guibert

The identification of oncogenic driver alterations that underlie sensitivity to small inhibitors has led to growing interest in identifying additional targetable oncogenes in nonsmall cell lung cancer. Although the therapeutic impact of the discovery of these alterations has now been widely demonstrated, the epidemiological data associated with each of these biomarkers remain insufficiently studied. In this review, we discuss the techniques used to discover each of these candidate oncogenes, their prevalence in nonsmall cell lung cancer, and briefly outline the epidemiological features of the major oncogenes and ways in which their identification can determine therapeutic strategies.


Author(s):  
Katja Kojo ◽  
Päivi Kurttio

Background: Indoor radon exposure is the second leading cause of lung cancer. Finnish radiation legislation obligates employers to measure indoor radon concentrations in workplaces, including schools and daycare centers, if they are in radon prone areas. Surveillance campaigns were conducted to ensure that the required radon measurements were performed and to gain knowledge on current indoor radon levels in daycare centers and schools. Methods: Daycare centers located in the high-radon risk municipalities were identified. Schools where indoor radon level measurements were obligatory but not performed, were identified. Results: Indoor radon measurements were performed in 633 daycare centers where the mean radon concentration was 86 Bq/m3 and the median 40 Bq/m3. The radon level was greater than 300 Bq/m3 in 8% (n = 49) of daycare centers. The radon measurements were performed in 1176 schools, which is 95% of the schools to be measured. The mean radon concentration was 82 Bq/m3 and the median 41 Bq/m3. The radon levels were greater than 300 Bq/m3 in 14% (n = 169) of the schools. Conclusions: The systematic surveillance campaigns by the radiation protection authority were very efficient in order to ensure that the measurements are performed in schools and daycare centers. The campaigns also reduced the radon exposure of employees, children, and adolescents, where necessary.


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