Where is lung cancer most common in the world

When determining the highest rates of lung cancer globally, epidemiologists don't usually use the incidence of death, also known as the mortality rate, to determine which countries have the highest rates of lung cancer.

This is because the death rate is influenced by many things, including the healthcare infrastructure of a country and the general health of the population. Developed countries like the United States, the United Kingdom, and France, therefore, have lower rates of lung cancer death rates compared to less wealthy countries like Montenegro, Serbia, and Bosnia-Herzegovina.

At the same time, the mortality rate is of less value when populations are small. Such is the case with a country like Samoa that has a population of less than , In some years, the death rate in Samoa may shoot to the top of the list if, say, 80 people die of lung cancer and the drop to the bottom if the number is below 10 as it did in the GBD research.

This is not to say that mortality is inconsequential in characterizing a country's disease burden. The mortality rate can help epidemiologists understand why people are dying at the rate they are—whether the cause is related to the healthcare infrastructure, prevalent forms of a disease, or even genetics —and provides governments the means to address and ideally mitigate any modifiable factors.

For the purpose of this article, countries with missing prevalence or incidence data were excluded from the top 20 list. Limiting processed foods and red meats can help ward off cancer risk.

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September 12, International Agency for Research on Cancer. In: Global Cancer Observatory. Updated March Global, regional, and national incidence, prevalence, and years lived with disability for diseases and injuries for countries and territories, a systematic analysis for the Global Burden of Disease Study American Cancer Society.

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Lung Cancer Survival Rates by Stage. Lung Cancer Survival by Stage and Type. Hungary Lung cancer incidence overall : Serbia Lung cancer incidence overall : Lung cancer mainly occurs in older people. Most people diagnosed with lung cancer are 65 or older; a very small number of people diagnosed are younger than The average age of people when diagnosed is about Each year, more people die of lung cancer than of colon , breast, and prostate cancers combined.

Varying trends in smoking largely dictate international patterns in lung cancer incidence and mortality. With declining smoking rates in developed countries and knowledge gains made through molecular profiling of tumors, the emergence of new risk factors and disease features will lead to changes in the landscape of lung cancer epidemiology.

Internationally, lung cancer continues to be the leading cause of cancer-related deaths in men and women [ 1 ]. A breakdown by level of economic development shows no differences in cancer deaths in men but a higher rate of lung cancer deaths in women in industrialized countries as compared with developing nations.

Among females in developing countries, lung cancer deaths lag behind those due to breast cancer [ 2 ]. Lung cancer incidence and mortality are tightly linked to cigarette smoking patterns. As smoking rates peak — generally first in men, followed by women — lung cancer incidence and mortality rise in subsequent decades before declining following the initiation of comprehensive tobacco control programs [ 3 , 4 , 5 ].

These trends have occurred earlier in industrialized countries as compared with the developing world. They exhibit a lower incidence of cancer but a higher mortality burden compared with developed countries. Reasons for these patterns include unequal access to healthcare leading to delayed diagnosis and treatment, environmental contamination, and sociocultural barriers [ 6 ].

In the US, the incidence of lung cancer in men peaked in the s, followed by a subsequent decline, with similar patterns in women following 20 years later [ 7 ]. Thun et al. Lung cancer deaths in men are now declining at an average of 2.

With regard to differences between racial and ethnic groups, non-Hispanic whites and blacks have the highest incidence and death rates [ 9 ]. In particular, black men have the highest mortality, approximately double that of Asian Americans, the group with the lowest cancer-specific mortality [ 7 , 10 ]. These racial and ethnic disparities are largely due to differences in cigarette smoking prevalence, as well as lower rates of resection and higher probability of advanced stage at diagnosis in minorities [ 11 , 12 , 13 ].

The UK has similar smoking and lung cancer incidence trends to the US. Male smoking prevalence peaked in the s to s, followed by a peak in lung cancer incidence in the s. Despite declining rates in both sexes, lung cancer remains the second most common malignancy in the UK [ 14 ]. In general, rates are highest in central and eastern Europe, but incidence throughout the continent has been declining in men since the early s. Exceptions include Norway, Finland, Spain, and France, where lung cancer rates have remained stable.

In women, rising lung cancer incidence has slowed in the US and UK, but rates continue to increase in central and eastern Europe [ 15 , 16 , 17 , 18 , 19 , 20 ]. These regional differences reflect earlier stages of the tobacco epidemic in countries such as Belarus, Hungary, Poland, and the Russian Federation [ 4 , 5 , 15 , 17 ]. Additionally, socioeconomic and educational inequalities, as well as diagnosis at later stages of disease, contribute to variability in lung cancer incidence and mortality within Europe [ 21 , 22 ].

Finally, similarly to the US, lung cancer survival is lower than that of any other common malignancies in Europe. Global lung cancer incidence and mortality. Global age-standardized incidence and mortality rates for lung cancer, 20 countries with the highest rates internationally. In Asia, Japan has high incidence and mortality rates from lung cancer, comparable to those of the US and Europe [ 25 ].

Men have had a higher incidence of lung cancer than women since the s and continue to comprise the majority of new lung cancer cases in Japan today, largely due to gender differences in smoking prevalence [ 26 ].

Conversely, mortality rates in women are lower in Japan than in other industrialized nations, perhaps due to the higher incidence of adenocarcinomas with mutations responsive to targeted therapies [ 27 ]. Brazil, Russia, India, China, and South Africa are recognized by their large and fast-growing economies [ 28 ]. One of the few South American countries with a cancer registry is Brazil, where tobacco smoking peaked in the s and lung cancer mortality in men peaked in and continues to rise among women [ 29 , 30 ].

Accordingly, Russia has among the highest lung cancer mortality rate in men of all European countries but among the lowest in women. Mortality is now declining, after peaking in the early s, but tobacco use remains a major barrier to effective cancer control [ 16 ].

Additional risk factors in Russia include environmental pollution and workplace exposures in nuclear facilities and asbestos mines [ 6 ]. Comparatively, lung cancer incidence and mortality rates in India are among the lowest in the world [ 4 ]. The most common cancers in men are head and neck, gastric, and esophageal cancers, attributed to high usage of smokeless tobacco; the most common cancers among women are cervical and breast.

One study in northern India noted that squamous cell lung cancer was the most common histology overall and among smokers [ 31 ]. In , the total number of new lung cancer cases in China was over , Lung cancer incidence and mortality is higher in eastern China and in urban areas, which has been attributed to westernization of lifestyle [ 33 ].

However, mortality rates are increasing faster in rural areas due to poor access to care [ 6 ]. Risk factors among Chinese women include secondhand smoking, air pollution, and domestic use of biomass fuels [ 35 ]. Reporting of cancer epidemiology in Africa is limited by the lack of reliable registries. Among countries on the African continent as whole, both incidence and mortality rates are low — lung cancer was the fifth most common site of cancer in African men and not even in the top 10 for women.

Lung cancer does have a high incidence in certain regions including the northern African countries of Western Sahara, Morocco, Algeria, Tunisia, and Libya, and it is the leading cause of cancer death in men in northern and southern Africa [ 36 ]. South America has a wide range of lung cancer incidence across countries and markedly higher rates in men compared with women.

The highest incidence and mortality in men can be found in Uruguay and in women of Venezuela and Argentina. Less populated countries such as Ecuador, Bolivia, and Guyana have very low age-standardized rates, just higher than those of central Africa and the Middle East [ 25 ].

The remainder of Asia has extremely diverse lung cancer incidences, which are nevertheless consistent within different regions. Asian countries closest to Eastern Europe such as Armenia, Turkey, and Kazakhstan have among the highest rates of lung cancer in the world. Korea and southeast Asia have slightly lower rates, and Middle Eastern countries including Yemen and Saudi Arabia have among the lowest lung cancer incidence rates in the world [ 25 ].

These notable regional differences reflect geographic trends in the tobacco epidemic [ 37 ]. Lung cancer was traditionally classified into two primary groups, small versus non—small cell type. This grouping was progressively specified with the use of histopathologic features and immunohistochemical markers, and now inroads are being made in distinguishing invasive adenocarcinomas from pre-invasive lesions.

Moreover, further knowledge about the molecular characteristics of lung cancers and the availability of targeted therapies has substantially impacted the classification of lung cancers. Adenocarcinoma is the most common histologic subtype of lung cancer in men and women [ 38 ].

Prior to the s, squamous cell lung carcinoma was the most common histologic subtype, particularly among men. Since then, the incidence of adenocarcinoma rose to be greater than that of squamous cell carcinomas in the US, Canada, many European countries, and Japan [ 26 , 39 ]. However, this switch has not yet been observed in other countries such as Spain and the Netherlands [ 39 ].

The higher rates of adenocarcinoma relative to squamous and small cell lung cancer are greater in women [ 4 ]. Consequently, the proportion of adenocarcinomas is rising in many countries in parallel to increased incidence of lung cancer in women.

These findings may reflect differences in the types of cigarettes including filtered and low-tar versions more frequently used by women as well as genetic predisposition and environmental exposures in female never-smokers [ 39 ]. In , the International Association for the Study of Lung Cancer, American Thoracic Society, and European Respiratory Society proposed a new adenocarcinoma categorization based upon histological evidence of invasion.

Invasive adenocarcinomas include a variety of patterns e. These tumors are distinguished histologically by squamous pearl formation, keratin production, and intercellular bridging. Historically, squamous cell lung cancer occurred more commonly as central lesions, but peripheral tumors are rising in incidence [ 41 ].

It has a strong association with smoking history and commonly causes paraneoplastic syndromes. In advanced stages of disease, this mutation predicts a more favorable prognosis and sensitivity to EGFR tyrosine kinase inhibitors TKIs such as erlotinib, gefitinib, and afatinib [ 44 ]. Conversely, KRAS mutations occur more commonly in smokers and appear to confer worse prognosis [ 42 ].

While no targeted therapeutics are currently available for this mutation, clinical trials are in progress to test drugs that target downstream effectors of activated KRAS [ 44 ]. ALK rearrangement are clinically important however, as this mutation creates a fusion product, most frequently with EML4, which predicts sensitivity to ALK tyrosine kinase inhibitors such as crizotinib and ceritinib [ 44 ]. Additionally, ALK-positive tumors have been associated with acinar or solid histological patterns with signet ring features [ 45 , 46 ].

Frequencies of common driver mutations in lung adenocarcinoma in the US and Europe. By overall frequency A and population group B. Data are derived from large clinicopathologic cohort studies published since and are representative of US and European populations. The myriad risk factors for lung cancer most commonly include lifestyle, environmental, and occupational exposures. The roles these factors play vary depending on geographic location, sex and race characteristics, genetic predisposition, as well as their synergistic interactions.

Cigarette smoking is the most recognized risk factor for developing lung cancer. While nicotine itself is not carcinogenic, there be as many as 55 substances in cigarette smoke that have been deemed carcinogenic by the International Agency for Research on Cancer including polycyclic aromatic hydrocarbons and 4- methylnitrosamino 3-pyridyl butanone NNK.

Their activation leads to the formation of DNA adducts and subsequent gene methylation, DNA sequence changes, DNA segment amplification or deletion, or whole chromosome gains or losses [ 48 ]. Relative risk of lung cancer in smokers as compared with smokers varies from to fold, and the degree of risk is dependent on number of cigarettes smoked daily and pack-years of smoking.

Cigar and pipe tobacco smoking are also associated with increased odds of developing lung cancer [ 49 ]. Secondhand smoke exposure also leads to a dose-dependent risk of lung cancer. The highest rates were in Europe, the western Pacific, and parts of Southeast Asia; the lowest rates were found in Africa. Over , deaths worldwide, most of them in women, were attributable to secondhand smoking in [ 50 ]. The largest numbers of estimated deaths in adults attributable to secondhand smoke, however, are not due to lung cancer but rather ischemic heart disease and asthma [ 50 ].

Electronic cigarettes have sparked much recent controversy over potential risks from long-term use, as well as their role in smoking initiation and potentially cessation [ 56 ]. The National Youth Tobacco Survey found the prevalence of ever-use of e-cigarettes among middle and high school students in the US to be 6.

Even more concerning, early research has shown that an e-cigarette vapor-conditioned media induced gene expression patterns in human bronchial epithelial cells concordant with that of cells exposed to a cigarette smoke-conditioned media [ 61 ].

Indoor emissions in these households contain high concentrations of polycyclic aromatic hydrocarbons, benzene, and other carcinogenic compounds [ 63 ]. Several studies have confirmed an increased lung cancer risk associated with biomass fuels, with one pooled analysis showing an odds ratio OR of 4. A meta-analysis including subjects from Europe and North America, in addition to Asia, reported similar trends in lung cancer risk with exposure to coal, biomass, and mixed fuels [ 62 ].

A cohort of newly diagnosed lung cancer cases was reported to have a prevalence of COPD as high as six-fold greater than matched smokers without cancer [ 67 ]. Furthermore, extent of emphysema on CT is an independent risk factor for lung cancer, as well as a predictor of cancer-specific mortality [ 69 , 70 ].

A recent pooled analysis of almost 25, cases from the International Lung Cancer Consortium also showed both lung cancer incidence and mortality to be significantly associated with emphysema [ 71 , 72 ].

Proposed mechanisms for the link between COPD and lung cancer include matrix remodeling and lung repair processes which lead to development of epithelial-mesenchymal transition and carcinogenesis. Additionally, several genome-wide association and candidate gene studies have identified associations between emphysema and lung cancer at several chromosomal loci, supporting that susceptibility to lung cancer may include COPD-related gene variants [ 73 ].

In a large meta-analysis, never-smokers with a history of chronic bronchitis, tuberculosis, or pneumonia were found to have an increased risk of lung cancer [ 71 , 74 ]. Exposure to asbestos is one of the most well-recognized occupational causes of lung cancer. Workers in asbestos mining and milling, shipbuilding, construction, textiles and insulation, and automobile repair are at the highest risk. Multiple mechanisms exist for carcinogenesis, including induction of oxidative damage and subsequent DNA deletions, somatic gene alterations, and enhanced delivery of tobacco carcinogens to the airway epithelium [ 75 ].

Markowitz and colleagues evaluated 2, North American insulators and found increased lung cancer risk to be associated with asbestos exposure rate ratio: 3. Diesel exhaust exposure has also been studied in trucking industry workers and coal miners. The SYNERGY project, a pooled analysis of 11 case-control studies conducted in Europe and Canada, which included 13, cases, showed that cumulative diesel exposure was associated with an increased lung cancer risk OR: 1.

Similar findings were obtained in studies conducted in the US trucking and non-metal mining industries [ 78 , 79 , 80 ]. Other occupations with an increased incidence of lung cancer include coal-mining [ 81 ], asphalt paving with coal tar exposure [ 82 ], chimney sweeping [ 83 ], and painting [ 84 ] although the risk appears to be lower than that of asbestos and diesel exhaust. Other organic and metal exposures that have been associated with lung cancer include beryllium, cadmium, chromium, silica, formaldehyde, benzo[a]pyrene, nickel, hard metal dust, and vinyl chloride, which often act synergistically with tobacco smoking [ 84 , 85 , 86 ].

European and American studies have evaluated the association of ambient air pollution with lung cancer risk. The ESCAPE study, an analysis of multiple cohorts from nine European countries, found particulate matter PM concentration in ambient air to be significantly associated with lung cancer risk hazard ratio [HR]: 1.

Studies in Canada [ 88 ], the Netherlands [ 89 , 90 ], and the UK [ 91 ] also found PM with median aerodynamic diameter less than 2. Arsenic occurring naturally in drinking water and food has been implicated in lung cancer [ 94 , 95 ]. Heck and colleagues evaluated lung cancer cases and found an OR of 2. Residential radon exposure is another known risk factor for lung cancer. An analysis of the CPS II cohort demonstrated a significant linear relationship between radon concentration and lung cancer mortality [ 97 ].

A Spanish case-control study found similar results, and also noted a strong interaction with tobacco OR: 2. Fruit and vegetable consumption have been associated with decreased lung cancer risk in current smokers; ingestion of cruciferous vegetables, in particular, has been inversely associated with lung cancer risk [ 99 , ]. An analysis of lung cancer tissue samples showed differentially expressed miRNAs among subjects with intake of quercetin-rich versus quercetin-poor fruit and vegetables [ ].

Many studies have attempted to evaluate the effects of vitamin levels and intake on lung cancer risk. Dietary and supplemental calcium intake has been shown to be inversely associated with lung cancer risk in female nonsmokers HR: 0. In addition, total iron intake was inversely associated with lung cancer risk in women, while total magnesium intake increased risk in men and current smokers; no significant association was found between copper, selenium, and zinc with lung cancer risk.

Johansson and colleagues found elevated serum vitamin B 6 and methionine levels associated with a lower risk for lung cancer in never, former, and current smokers in Europe [ ]. Conversely, the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study, revealed a greater incidence of lung cancer and overall mortality in male smokers supplemented with 20mg b-carotene daily [ ]. Moreover, the USPSTF recently concluded that there is insufficient evidence to recommend any vitamins, minerals, and multivitamin supplementation for lung cancer prevention [ ].

Genetic factors leading to increased susceptibility to lung cancer have been poorly studied. First-degree relatives of patients with lung cancer are at increased risk, even after adjusting for smoking habits [ ]. A meta-analysis of 28 case-control studies and 17 observational cohort studies of individuals with positive family histories found a RR of 1. Additionally, genome-wide association studies have suggested susceptibility loci on various chromosomes, including 5p Other studies have identified polymorphisms in various enzymes such as cytochrome p enzymes and DNA repair genes [ ], as well as germline mutations in the EGFR [ ].

Except for smoking cessation, perhaps the highest reduction in lung cancer mortality rates is related to diagnosis at early stage followed by surgical resection. Ongoing European trials will provide additional critical information regarding the potential benefits of lung cancer screening [ , ]. However, CT screening is associated with high rates of positive findings and may lead to identification of some lung cancers with low aggressiveness [ ]. Thus, better risk stratification using prediction models or biomarkers of lung cancer risk, as well as a better understanding of the biologic characteristics of aggressive cancers is required to maximize the benefit of screening.

Even within smokers, lung cancer risk varies considerably based on factors such as age, quantity and duration of smoking, and environmental exposures [ 3 ]. There is an ongoing effort to stratify lung cancer risk to identify individuals best suited for lung cancer screening or refine eligibility for prevention trials. Several models based on sociodemographic characteristics, smoking, and other risk factors have been empirically derived using relatively large cohorts [ , ].

Among these, the Bach model was developed using information from 18, subjects in the Carotene and Retinol Efficacy Trial, which followed heavy smokers and asbestos-exposed workers from to [ ]. This model was validated in the Alpha-Tocopherol Beta-Carotene Cancer Prevention Study and was found to underestimate year absolute lung cancer risk while having a discriminatory power comparable to breast cancer risk models [ ].

Likewise, the Spitz model was derived and validated in a cohort of 1, lung cancer patients and 2, matched controls from a single tertiary center. Risk factors among current and former smokers, including exposure to environmental tobacco smoke, dust, fumes, chemicals, history of emphysema, and family history of cancer, predict an increased risk for cancer [ ].

Finally, the Liverpool Lung Project model, validated in multiple independent populations, is based on data about smoking duration, history of pneumonia or cancer, family history of lung cancer, and asbestos exposure to predict five-year lung cancer risk [ , ]. Recent research has focused on identifying biomarkers of lung cancer risk, aggressive behavior among early cancers, and prognosis.

These biomarkers may be produced by neoplastic cells themselves, the tumor microenvironment, or the host. A variety of methods to identify biosignatures utilizing tissue- and biofluids-based assays have been tested and include genome-wide association studies GWAS , epigenetics, microRNA, and proteomics [ ]. Using GWAS, several single nucleotide polymorphisms SNPs have been identified on specific chromosomal loci — such as the 15q25 locus — that are associated with tobacco exposure and lung cancer [ ].

It remains to be seen whether these SNPs can be utilized in the clinical setting to assess lung cancer risk.