A few limitations of the present study should be mentioned. First, air pollution measurement campaigns were implemented between 2008 and 2011, after the follow-up period of most cohorts (; ). As a consequence, this study relies on the assumption that the intracohort spatial distribution of air pollution has not dramatically changed in the last 10–15 years and that the land-use model predictions are thus representative of the baseline spatial contrasts for all the cohorts investigated. Several studies in the literature support this assumption over periods of about 10 years (; ). In addition, within the ESCAPE project many efforts were made to back-extrapolate air pollution concentrations, taking into account long-term time trends (see Supplemental Material, “Methods,” pp. 3–13), and analyses relating back-extrapolated data to the health outcomes showed no clear differences in the results compared with original data (data not shown). We also performed an exploratory analysis to evaluate whether the association between PM2.5 and stroke incidence differed according to accrual time, under the hypothesis that the assumption of stable spatial distribution of air pollution over time could be more valid for more recent cohorts: We did not find meaningful differences in the association estimates across cohorts according to accrual time (data not shown). Second, our approach exploited only within-study area contrasts, which limited the exposure contrast, but decreased the risk of potential confounding when comparing diverse cohorts from different countries. Third, the data available to adjust for confounding were somewhat different from cohort to cohort, allowing the possibility of different degrees of residual confounding in the cohort-specific results. However, the most relevant cardiovascular risk factors (smoking, diabetes or hypertension, BMI, physical activity) were available in almost all the cohorts, and thus severe bias in the effect estimates due to residual confounding is unlikely. Finally, we did not consider the possible impact of loss to follow-up (drop out or death) on the findings. Air pollution exposure is an established cause of mortality, so that older participants are likely to represent a population that is “selected” such that those who sustained higher exposures are more likely to have characteristics (genetic or otherwise) that place them at lower risk for stroke, resulting in underestimation of the causal relation of exposure with stroke risk. However, given the small relative risk of the air pollution–mortality association (i.e., HR 3 increase in PM2.5 or 10-μg/m3 increase in PM10 or NO2 as reported by ), this underestimation is likely to be small.
In any case, the result for never-smokers is relevant because it indicates limited possibility of residual confounding from smoking and that the relative effect of ambient air pollution on stroke incidence is more easily detectable in the absence of a strong risk factor for stroke, such as active smoking.
This study has several limitations. We used exposures based on the baseline home address as a proxy for actual exposures over time. However, a number of studies have also demonstrated that land-use regressions, such as the one used here, are quite robust to historical changes (; ; ). Our inability to incorporate changes in residence during the study period would have induced further exposure misclassification. Another limitation is that we were not able to adjust our analyses of NO2 (due to violations in the required assumptions) and the traffic proximity and volume measures (due to a lack of data in the validation study) for measurement error. The high β12σ2 for NO2 is likely attributable to the presence of indoor sources or low air exchange rates, which have been consistently observed in other studies (; ; ; ; ). Given the differences in measurement error for PM2.5 and BS, it is not possible to determine the potential magnitude error that would be observed for NO2. We are also not able to quantify the impact of indoor sources of NO2 on lung cancer risk. Therefore, our NO2 associations should be treated with caution and interpreted only as the ambient effects of these exposures. Last, as with all studies, residual confounding is a concern. Our study was not able to update potential confounders, such as smoking or diet, after baseline, and we were missing information on potential confounders such as secondhand smoke and occupation for around 10% of the study participants.
Although we observed HRs of different magnitudes for the different lung cancer subtypes we examined, there was no statistically significant heterogeneity among the subtypes. Differences of effect among subtypes are of great interest, but to date only a limited number of studies have examined histological subtype–specific effects. This interest in differences by subtype is motivated by differences in risk observed with exposures to cigarette smoking. For example, small-cell carcinoma, squamous-cell carcinoma, and adenocarcinomas have been the subtypes most closely associated with cigarette smoking (; ). Stronger associations with various pollutants have been observed for adenocarcinomas and squamous-cell carcinomas. Specifically, in ESCAPE, elevated HRs were observed in models of PM2.5 exposure restricted to these two subtypes when compared with models of all cases (). In a case–control study in Canada, subtype-specific results for PM2.5 and NO2 were mixed, with a suggestion of a larger risk for adenocarcinomas compared with other subtypes (). Positive associations with exposures to PM were also observed for adenocarcinomas compared with all lung cancer cases in a study of U.S. nurses ().
Although there was little evidence of effect modification by follow-up period, our results had HRs of greater magnitude and more were statistically significant compared with our previous findings in this cohort (). For example, in the present analysis, the HR for BS was 1.16 (95% CI: 1.02, 1.32, per 10 μg/m3), compared with an equivalent HR of 1.03 (95% CI: 0.78, 1.34) in our previous analysis. Additionally, we observed HRs > 1 with exposures to PM2.5 and NO2, which were not observed in the previous analysis. However, although we had previously observed differences in these associations by smoking status, we did not observe statistically significant differences by smoking status in the present analysis.
This collection is meant to feature more than 100 anthropology research paper examples. Since its emergence as a scientific discipline in the middle of the 19th century, anthropology has focused on the study of humankind in terms of science and reason, as well as logical speculation. Within a comprehensive and interdisciplinary framework, anthropology aims for a better understanding of and proper appreciation for the place of our species within earth history and organic development. As such, the scientific theory of biological evolution has been indispensable for giving meaning and purpose to the awesome range of empirical facts and conceptual insights that now constitute the rich content of present-day anthropology. Furthermore, cross-cultural studies emphasize the vast differences among human groups from the perspectives of material culture, social behavior, languages, and worldviews. Browse
The topic of tobacco is extremely important today, because the humanity still can not cope with this problem. So, students from high school to college and university are offered to write a research paper on the topic. A perfect research paper on tobacco use should be informative and convincing. There should be detailed descriptions of the effect of tobacco use on the human body, as well as analysis of the cause of smoking and its popularity among people.
Then, parents’ example is quite effective in this occasion, because the majority of young smokers tried their first cigarette following their parents’ habit.
For quite a long period of time people did not know about the negative effect of tobacco on the human health. The harms thought or known to caused by using tobacco include diseases affecting the heart and lungs, with smoking being a major risk factor for heart attacks, strokes, chronic obstructive pulmonary disease (COPD), emphysema, and cancer (particularly lung cancer, cancers of the larynx and mouth, and pancreatic cancers). Evidently, tobacco is dangerous for human organism but still millions of people in the world can not give up smoking, because it is severely advertised by the producers of cigarettes who make much money on it.
Students who are required to prepare a research paper are expected to read a lot about tobacco and its use, its effect on the human body and the world economics. Before writing your own paper it will be useful for you to read free sample research papers on tobacco industry to broaden your horizons and understand the problem deeper. Moreover, while reading a free example research paper on tobacco advertising you start to realize how to compose the paper properly, how to organize your thoughts in a good way and to provide evidence which support your point of view.
Mass culture has created an image of the hero who is always able to cope with any problem and he smokes every time there is an occasion for it. Adolescents, especially young men think that smoking solves problems and the bad example of movies and advertisements influences the human mind. It does not worth mentioning that more than 90% of adult smokers got used to this habit in adolescence, so it is important to protect teenagers from smoking in order to save their health in future. Teenagers who smoke about 10 cigarettes per day are more likely to suffer from depression and anxiety disorders, cancer, diseases related with digestion, cardiovascular and respiratory systems.
The student who studies the issue about teenage smoking is supposed to learn the roots of this problem, the social categories of adolescents who start smoking early, the factors which cause smoking, etc. Finally, one should compare different countries and social groups of smokers and study the solutions to this problem all over the world presenting the most effective methods in the term paper.