Article

Causes of cancer in the world: comparative risk assessment of nine behavioural and environmental risk factors.

Harvard School of Public Health, Boston, MA 02115, USA.
The Lancet (Impact Factor: 39.21). 12/2005; 366(9499):1784-93. DOI: 10.1016/S0140-6736(05)67725-2
Source: PubMed

ABSTRACT With respect to reducing mortality, advances in cancer treatment have not been as effective as those for other chronic diseases; effective screening methods are available for only a few cancers. Primary prevention through lifestyle and environmental interventions remains the main way to reduce the burden of cancers. In this report, we estimate mortality from 12 types of cancer attributable to nine risk factors in seven World Bank regions for 2001.
We analysed data from the Comparative Risk Assessment project and from new sources to assess exposure to risk factors and relative risk by age, sex, and region. We applied population attributable fractions for individual and multiple risk factors to site-specific cancer mortality from WHO.
Of the 7 million deaths from cancer worldwide in 2001, an estimated 2.43 million (35%) were attributable to nine potentially modifiable risk factors. Of these, 0.76 million deaths were in high-income countries and 1.67 million in low-and-middle-income nations. Among low-and-middle-income regions, Europe and Central Asia had the highest proportion (39%) of deaths from cancer attributable to the risk factors studied. 1.6 million of the deaths attributable to these risk factors were in men and 0.83 million in women. Smoking, alcohol use, and low fruit and vegetable intake were the leading risk factors for death from cancer worldwide and in low-and-middle-income countries. In high-income countries, smoking, alcohol use, and overweight and obesity were the most important causes of cancer. Sexual transmission of human papilloma virus is a leading risk factor for cervical cancer in women in low-and-middle-income countries.
Reduction of exposure to key behavioural and environmental risk factors would prevent a substantial proportion of deaths from cancer.

3 Bookmarks
 · 
406 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Tobacco smoking continues to be a leading cause of disease and mortality. Recent research has confirmed the important role of nicotinic acetylcholine receptor (nAChR) gene cluster on chromosome 15q 24-25 in nicotine dependence and smoking. In this study we tested the association of smoking initiation, age at onset of daily smoking, and heaviness of smoking with five single nucleotide polymorphisms (SNPs) within the CHRNA5-CHRNA3-CHRNB4 cluster. The group of 389 adult subjects of European ancestry from the north of Poland, including 212 ever (140 current and 72 former) and 177 never smokers with mean age 49.26, was genotyped for rs16969868, rs1051730, rs588765, rs6495308, and rs578776 polymorphisms. Distributions of genotypes for rs16969868 and rs1051730 were identical so they were analyzed together. Further analysis revealed the association between rs16969868-1051730 (OR = 2.66; 95% CI: 1.30-5.42) and number of cigarettes smoked per day (CPD) with heaviness of nicotine addiction measured by the Fagerström Test for Nicotine Dependence (FTND) (OR = 2.60; 95% CI: 1.24-5.43). No association between these polymorphisms and other phenotypes was found. Similarly, the association between rs588765, rs6495308, rs578776, and analyzed phenotypes was not confirmed. This study provides strong evidence for the role of the CHRNA5-CHRNA3-CHRNB4 cluster in heaviness of nicotine addiction.
    BioMed Research International 01/2015; 2015:350348. · 2.71 Impact Factor
  • Journal of Food Composition and Analysis 06/2013; 30(2):67-72. · 2.26 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The level of atmospheric oxygen, a driver of free radical damage and tumorigenesis, decreases sharply with rising elevation. To understand whether ambient oxygen plays a role in human carcinogenesis, we characterized age-adjusted cancer incidence (compiled by the National Cancer Institute from 2005 to 2009) across counties of the elevation-varying Western United States and compared trends displayed by respiratory cancer (lung) and non-respiratory cancers (breast, colorectal, and prostate). To adjust for important demographic and cancer-risk factors, 8–12 covariates were considered for each cancer. We produced regression models that captured known risks. Models demonstrated that elevation is strongly, negatively associated with lung cancer incidence (p < 10^−16), but not with the incidence of non-respiratory cancers. For every 1,000 m rise in elevation, lung cancer incidence decreased by 7.23 99% CI [5.18–9.29] cases per 100,000 individuals, equivalent to 12.7% of the mean incidence, 56.8. As a predictor of lung cancer incidence, elevation was second only to smoking prevalence in terms of significance and effect size. Furthermore, no evidence of ecological fallacy or of confounding arising from evaluated factors was detected: the lung cancer association was robust to varying regression models, county stratification, and population subgrouping; additionally seven environmental correlates of elevation, such as exposure to sunlight and fine particulate matter, could not capture the association. Overall, our findings suggest the presence of an inhaled carcinogen inherently and inversely tied to elevation, offering epidemiological support for oxygen-driven tumorigenesis. Finally, highlighting the need to consider elevation in studies of lung cancer, we demonstrated that previously reported inverse lung cancer associations with radon and UVB became insignificant after accounting for elevation.
    PeerJ. 01/2015; 2:e705.

Full-text (2 Sources)

Download
54 Downloads
Available from
May 28, 2014