Abstract

Lung cancer in never-smokers (LCINS) has become an escalating global crisis, accounting for 10–25% of all lung cancer cases. The incidence of this condition is rising so rapidly that if considered a separate entity, it would rank amongst the top ten most common cancers in the world.  

While clinical focus has historically targeted tobacco-related lung cancer with the declining rate of smoking, LCINS has become a growing concern. Current clinical research demonstrates that LCINS results from a complex interplay of cultural, genetic, environmental and socioeconomic variables which vary by ethnicity or environment. This article aims to consider a refined form of treatment by comparing, analysing and evaluating data from major lung cancer studies such as NLST (the National Lung Screening Trial) and IPASS (IRESSA Pan-Asia Study) and also highlighting the impact of proper treatment tailored to the patients and lack of inclusion of the most at-risk ethnicities such as Asian women and Hispanics. The analysis reveals that some enrolment criteria act as a systemic barrier for minorities; furthermore, it also reveals that through specialised and tailored treatments, such as TKIs (Tyrosine Kinase Inhibitors), the results become significantly more successful.

Introduction

Lung cancer in never-smokers (LCINS) is an increasingly significant public health concern, accounting for approximately 10–25% of all lung cancer cases worldwide and representing a leading cause of cancer-related mortality (de Alencar et al., 2022). This trend coincides with rising rates of smoking cessation, highlighting the growing importance of non-tobacco-related risk factors in lung carcinogenesis. In ethnic minorities these factors include cultural, environmental, genetic, and socioeconomic influences (Yadav et al., 2022; National Centre for Atmospheric Science, 2026; Ha et al., 2015; Chen et al., 2024).

Although numerous therapeutic strategies have been developed and demonstrated efficacy in LCINS, many of these interventions were derived predominantly from studies conducted in Western, primarily White populations. For example, the National Lung Screening Trial, widely regarded as one of the most influential studies in the advancement of lung cancer treatment, had a participant population that was 90.8% White, 4.4% Black and only 2% Asian (The National Lung Screening Trial Research Team, 2011). Consequently, treatments based on genetic mutations or biological mechanisms identified in these cohorts may not be generalisable to ethnic minority groups, such as East Asians and individuals of African descent, in whom non-small cell lung cancer (NSCLC) exhibits different prevalence patterns and potentially distinct etiologies. This poses significant risks to ethnic minorities, including reduced efficacy, safety issues due to metabolic or genetic differences and the widening of health disparities. It leads to inaccurate diagnoses, inappropriate dosing and ignores cultural/systemic factors that affect treatment outcomes (Chauhan et al., 2020).

To address this gap, this article examines the key drivers of non‑small cell lung cancer (NSCLC) in underrepresented populations, including cultural practices (high‑temperature cooking and incense burning), environmental exposures (PM2.5 pollution), genetic predispositions (EGFR and KRAS mutations) and socioeconomic factors such as proximity to pollution, occupational hazards (asbestos and silica exposure) and inadequate infrastructure. It critically evaluates the current evidence on available treatments, including the National Lung Screening Trial and the IRESSA Pan-Asia Study (IPASS), and proposes tailored therapeutic strategies to improve outcomes. These strategies include low‑dose helical computed tomography for early detection, AI-assisted analysis of high-quality biopsies to assess mutation progression and guide treatment selection, and the use of targeted inhibitors for mutations commonly found in ethnic minority populations (such as the EGFR and KRAS mutations). By incorporating a more inclusive understanding of the disease, we aim to develop interventions that are both effective and broadly applicable across diverse patient populations.

CULTURE

Culture is a fundamental aspect of society and can vary across different ethnic groups and minorities. There have been many studies to show that cultural aspects can significantly increase lung cancer risk in never-smokers. 

In many Asian cultures, cooking involves high-temperature stir-frying, wok cooking and the use of certain oils like soybean or rapeseed oil (Kim et al., 2014; Cheng et al., 2021). When cooked in high temperatures, these oils can emit fumes that are high in polycyclic aromatic hydrocarbons (PAHs) (Li, Pan & Wang, 1994). PAHs cause lung cancer primarily because they are metabolised in the body into highly-reactive compounds that bind to DNA, causing mutations and initiating tumour growth. These lipophilic compounds enter cells, where enzymes (CYP1A1/1B1) convert them into diol-epoxides or radical cations, forming DNA adducts that disrupt genetic stability and damage tumour suppressor genes like p53 (Moorthy et al., 2015). This dose-response relationship between lung cancer risk and years of cooking fumes exposure, particularly with high temperature frying, can explain why East Asia (often China) has a higher prevalence of lung cancer in never-smokers as Chinese-style cooking often involves volatilisation of oils, potentially exposing people to more fumes than cooking methods from other regions of the world (Li et al., 1994; Kim et al., 2014).

Incense, as coils, cones, powders and sticks, is widely used for religious and cultural practices within many ethnic minorities (primarily across Asia – including India, China, Japan, Korea, Vietnam, Thailand and Tibet) (Lam et al., 2024; Reality Pathing, 2024). Usage includes meditations, celebrations and deodorisations, in addition to spiritual and ancestral worship (Lam et al., 2024). Burning incense releases significant amounts of PM2.5, which consist of fine particulate matter, toxic gases, heavy metals and organic compounds (PAHs, benzene, formaldehyde) (Yadav et al., 2022). These pollutants are said to affect people in the same way that secondhand smoke does, with an average of 45 mg/g of particulate matter being released from incense burning compared to 10 mg/g from a cigarette (Mannix et al., 1996). In never-smokers, these pollutants can cause lung cancer as they penetrate deep into the lungs, triggering inflammation, causing genetic mutations in lung cells and promoting tumour growth, particularly with long-term exposure in poorly ventilated spaces (Stem Cell Regeneration Center, 2025). Although evidence on the link between incense burning and lung cancer in never-smokers is inconsistent, with many studies finding no significant association compared to the stronger link found in smokers, the possible health hazards it poses must not be disregarded (Friborg et al., 2008; Lam et al., 2024).

ENVIRONMENT

Environmental factors have been strongly linked to the rising incidence of lung cancer among never-smokers as smoking rates decline while exposure to environmental pollutants continues to increase (Lüthi, 2025). Ethnic minority groups are disproportionately exposed to these environmental conditions as they are more likely to live in areas with high levels of nitrogen dioxide (NO₂) and particulate matter, which may increase their risk of developing lung cancer (National Centre for Atmospheric Science, 2026). This is primarily due to structural racism, residential segregation and socioeconomic inequalities. These factors lead to higher exposure to industrial pollution, traffic-related air pollution (NO2, PM2.5), lower housing quality and increased occupational risks (asbestos, silica) (United States Environmental Protection Agency, 2021; Dillard, 2023).

 A prior study suggests that air pollution significantly contributes to lung cancer in individuals who have never smoked, with a particularly strong impact observed among East Asian women (Myers et al., 2021). This is largely because many Asian countries experience substantial industrial pollution and poor air quality (Muhammad, Elliott & Ibanez, 2023). In Central Asia in particular, air pollution levels frequently surpass the World Health Organisation guidelines for PM2.5, ozone and nitrogen dioxide (NO₂) (Health Effects Institute, 2025). In such countries, the burning of solid and fossil fuels (such as coal, oil and gas) accounts for approximately 20–30% of the estimated ambient PM2.5 concentrations (Health Effects Institute, 2025). Extending from the effects of incense burning, PM2.5 encourages the proliferation of lung cells that harbour cancer-causing mutations (University College London Hospitals NHS Foundation Trust, 2023). Once inside the body, these harmful substances stimulate macrophages to generate reactive oxygen species (ROS). The resulting oxidative stress damages DNA and causes inflammation in tissues, leading to irregular gene expression and a heightened risk of cancer (Chen et al., 2024). It could therefore be said that chronic exposure to air pollution (an issue most common in Asia) increases the incidence of lung cancer (Thangavel et al., 2022). Addressing these risk factors is essential to reducing the overall burden of lung cancer in vulnerable populations.

Nonetheless, it is true that environmental factors do not cause lung cancer alone. Instead, they accelerate lung cancer in never-smokers by acting on pre-existing genetic vulnerabilities, inducing chronic inflammation and DNA damage that trigger dormant mutations to drive tumour development (Lung Cancer Foundation of America, 2025). This means that the never-smoker must first have that genetic vulnerability for their chance of lung cancer to increase after exposure to air pollution.

GENETICS

Cancer is caused by genetic mutations that turn healthy cells into malignant tumour cells, driven by a combination of factors including age, genetic predisposition and environmental/lifestyle exposures (Gale, 2024). More specifically, never-smokers develop lung cancer due to mutations later in life, such as mutations in the EGFR (epidermal growth factor receptor) or ALK (anaplastic lymphoma kinase) genes. These are not typically inherited but develop over time, frequently seen in never-smokers, especially in certain demographics like women and ethnic minorities like East Asians and, to a lesser degree, Hispanic populations (American Cancer Society, 2025). In these populations, genetic risk is often linked to a high prevalence of oncogene-addicted, actionable driver mutations rather than the high mutational burden caused by smoking (Ha et al., 2015; James et al., 2023). Notably, approximately 50–63% of lung adenocarcinomas in non-smoking Asian women harbor EGFR mutations – much higher than the 19% observed in non-smoking Western populations (Ha et al., 2015). The most common alterations are exon 19 deletions and the L858R mutation in exon 21, which promote uncontrolled cell growth and are highly responsive to targeted tyrosine kinase inhibitors (TKIs) (Phillips, 2025; Tian et al., 2025; Dogan et al., 2012). Other important driver alterations include ALK rearrangements, which are commonly observed in never-smokers, especially among East Asian patients (reported in 7–12% of cases in some studies), and are often linked to younger age and solid-pattern adenocarcinoma (Ha et al., 2015; Phillips, 2025). ROS1 and RET fusions occur in a smaller group, predominantly in never-smoking Asian women (Ha et al., 2015). 

Furthermore, there are African ancestry-associated variants. Research indicates that a higher proportion of West African genetic ancestry correlates with an increased prevalence of EGFR mutations. Additionally, novel variants in CHRNA5 (15q25.1) and TERT (5p15.33) have been associated with elevated lung cancer risk among African American populations (Enesco, 2026). KRAS mutations are generally more frequent in smokers, but certain KRAS variants (such as G12Asp) can occasionally appear in never-smokers (Dogan et al., 2012). They occur in approximately 17%–22% of African American patients with non-small cell (NSCLC) lung cancer and permanently activate the KRAS protein, which acts as a “switch” for cell signalling driving uncontrolled cell proliferation, growth and survival (Reinersman et al., 2011; Our Cancer Stories, 2024).

Lastly, there are Hispanic/Latino-specific variants that can increase the risk of lung cancer in never-smokers. Studies have identified distinct genetic variants in DNA repair genes (such as ERCC2 and XRCC1) and in carcinogen-metabolising genes (e.g., CYP1A1) that influence risk. Notably, certain variants, such as the ERCC2 haplotype, appear to confer a protective effect in never-smokers (Zhou et al., 2003; Castañeda‑González et al., 2025; San Jose et al., 2010).

SOCIOECONOMICS

Ethnic minority groups often experience lower socioeconomic status compared to the majority population. Such disparities in social position and economic resources can increase the vulnerability of these groups to various health conditions (including lung cancer in never-smokers) due to systemic inequalities in housing, poverty, disadvantageous employment and local environments (British Medical Association, 2026; People’s Health Trust, 2026).

Socioeconomic factors often result in higher residential concentrations in areas with elevated pollution levels, with specific groups, such as Black communities, disproportionately situated in locations with greater toxic environmental contamination (Mohai et al., 2009; Health Foundation, 2024). Furthermore, economically disadvantaged communities and underdeveloped regions are also more likely to be located near industrial zones, major transportation networks and hazardous waste sites, further exacerbating their exposure to environmental hazards (Lancaster University, 2021). As discussed in the section on environmental impacts, exposure to such pollutants (including PM2.5) can elevate the risk of lung cancer in never-smokers by inducing pulmonary inflammation. This inflammation can activate otherwise dormant lung cells that carry oncogenic mutations. The interaction between these mutations and the inflammatory response may promote uncontrolled cell proliferation, ultimately resulting in tumour formation (University College London Hospitals NHS Foundation Trust, 2023).

Beyond the risks posed by residential pollution, many ethnic minority individuals take on manual labour jobs to secure income, which can inadvertently increase their exposure to occupational pollutants. Black populations, in particular, experience higher occupational exposure to carcinogens due to disproportionate representation in manual labour industries. Additionally, they are more likely to encounter elevated levels of silica and asbestos (Juon et al., 2021). Exposure to silica and asbestos elevates the risk of lung cancer in never-smokers by inducing chronic inflammation, pulmonary fibrosis and the production of reactive oxygen species (ROS). These persistent inhaled particles inflict DNA damage in lung epithelial cells, initiating abnormal repair processes that can ultimately result in malignant tumour formation (Sato et al., 2018; Selby, 2025).

As previously discussed, never-smoking women, particularly in East Asian communities, face elevated lung cancer risk due to chronic exposure to cooking oil fumes that release polycyclic aromatic hydrocarbons (PAHs). Due to their socioeconomic state, such ethnic minority populations may live in housing where there is inadequate ventilation and the absence of kitchen fume extractors, particularly in older homes, and as a result lead to substantial inhalation of particulate matter and potential carcinogens by non-smoking women (Kim et al., 2015). Inhaled carcinogens in poorly ventilated kitchens, such as polycyclic aromatic hydrocarbons (PAHs) from cooking fuels (coal) and fine particulate matter (PM2.5) from cooking oil fumes (COFs), cause DNA damage and chronic inflammation, leading to a 49–69% increased risk of lung cancer in never-smokers, particularly via adenocarcinoma. These toxins trigger mutations and fuel tumour growth in lung cells (Kim et al., 2015). These factors create a cycle where socioeconomic deprivation causes higher environmental exposure, resulting in higher illness rates, which in turn are harder to treat due to limited access to advanced, expensive and specialised care (World Health Organisation, 2023).

The Significance and Impact of Previous Studies on Lung Cancer in Never-Smokers 

While the socioeconomic barriers and environmental triggers provide the foundation of the overall risk of developing lung cancer, they also influence who gets the opportunity to be studied. In the past, massive clinical trials were funded to study the “high-risk” groups, which were the smokers. This resulted in a blind spot regarding the 10–15% and growing number of LCINS of which the East Asian population demonstrate the highest prevalence of actionable mutations, proved by a 2014 study (Shi et al., 2014) which identified an overall EGFR mutation rate of 60.7% in Asian non-smoker patients with adenocarcinoma. The clinical blind spot resulted in the benefit of past medical advancements/trials not being equally distributed and instead is dictated by the patient’s access to modern medicine. 

When considering past studies regarding LCINS, the National Lung Screening Trial proved to be particularly useful in the detection of lung cancer. This study included 53,454 persons at high risk of lung cancer (The National Lung Screening Trial Research Team, 2011). The study showed that by screening the high-risk patient population with low-dose computed tomography scans, lung cancer mortality was reduced by 20% compared to the standard chest X-ray. This benefitted the field of medicine as it was the first time that lung cancer could be detected early enough to be cured. However, while the study was a victory for the overall patient population, it also highlighted the massive “benefit gap” that exists for ethnic minorities. This benefit gap refers to the difference in: poverty, as poverty and deep poverty rates are higher in many ethnic minority groups; social security, as ethnic minority families are more likely to receive benefits; and work, as working-age adults from ethnic minority backgrounds are more likely to be unemployed or working in low-paying insecure jobs (Joseph Rowntree Foundation, n.d.). This was done by the study’s definition of the “high-risk” patient population.

Research conducted by Aldrich et al. (2019) highlighted a critical disparity: ethnic minorities, particularly Black and Asian populations, often develop lung cancer at a younger age and/or without a heavy smoking history. As the NLST utilised criteria based primarily on White smoking patterns, these minorities were systematically excluded from the trial even though they made up roughly 13% of the population. Statistical evidence points to a dramatic disparity in the demographics of the NLST participants. A staggering 90.8% of the NLST participants were White, while only 4.4% were Black and a minuscule 2% were Asian (The National Lung Screening Trial Research Team, 2010). Their analysis of the Southern Community Cohort found that Black smokers were diagnosed with a median of 25.8 pack-years compared to 48.0 pack-years in White smokers (Aldrich et al., 2019). Consequently, the NLST’s strict 30 pack-year criteria functioned as a barrier rather than a gateway. Since these minority groups were not represented in the NLST trial, the “standard” for lung cancer screening was never validated for the unique biological and environmental characteristics. In the case of the Asian non-smokers, the exclusion was absolute. The NLST provided no means for the detection of the EGFR-driven lung cancer as the trial’s eligibility was based exclusively on heavy tobacco use, which largely ignores the primary risk factor for non-smoking Asian females. By the time these patients were diagnosed, they had often already progressed to the late stages of the disease, thus failing to reap the 20% mortality rate savings (The National Lung Screening Trial Research Team, 2010).

Ultimately, the NLST shows that medical breakthroughs can unintentionally widen health gaps if the study rules do not account for the biological diversity of the entire population. Without the consideration that the onset of lung cancer presents differently in different ethnicities, the NLST inadvertently created a system in which the detection of the disease was a privilege of the majority, while the minority had to endure the consequences of the disease in its late stages. 

Where the NLST demonstrated the failure of early detection, the IRESSA Pan-Asia Study (IPASS), published in 2009, changed the treatment plan for those already diagnosed with late-stage lung cancer (Mok et al., 2009). The worldwide standard of care for non-small cell lung cancer has been “platinum-based doublet chemotherapy”, which damages the body by attacking healthy cells as well as cancer cells. The IPASS trial marked a turning point in the treatment of NSCLC as it was the first trial to specifically recruit a group of 1,217 NSCLC patients in East Asia, either never-smokers or light smokers with adenocarcinoma histology, to compare the efficiency of a targeted tyrosine kinase inhibitor to chemotherapy (Mok et al., 2009). The trial was groundbreaking because, for the subgroup of those patients whose EGFR mutation was positive, the targeted therapy gave a significantly longer PFS (progression-free survival) than chemotherapy, with a hazard ratio for disease progression or death of 0.48, effectively a 52% reduction in the risk of disease progression (Mok et al., 2009). The objective response rate for the targeted therapy group was a phenomenal 71.2%, nearly twice that of the chemotherapy group. 

However, the true significance of IPASS is that it discovered the “genetic divide” between patients with and without the EGFR mutation. In patients who did not have the EGFR mutation, the IPASS study found that chemotherapy as a matter of fact did work better than the drug. This proved that “Asian ethnicity” or “never-smoking status” is just a “proxy” variable, while the true determinant of whether the drug or chemotherapy is effective is the molecular biology of the tumour itself (Mok, et al., 2009). The IPASS provided an alternative route to those with the specific gene mutation EGFR. It did not just improve outcomes; it proved that treating a patient based on their genetic “driver mutations” is the only way to obtain true clinical benefit. 

While there have been significant benefits to the Asian populations, there have not been significant benefits to Black and Hispanic never-smokers because of the “data desert” and lack of evidence that continues to exist in clinical studies. While Black Americans suffer one of the highest burdens of lung cancer mortality, they represent only an estimated 2–5% of the patients in clinical trials that determine what is beneficial to them (Nemala et al., 2023). The consequences of this exclusion in the real world are illustrated by a 2019 study which highlighted the issues with the criteria, such as African American smokers diagnosed with lung cancer had significantly lower median smoking pack-years compared with White smokers (Aldrich et al., 2019). By examining the health records of thousands of patients, the researchers found that the established screening criteria (based on the White smoking patterns) would have identified 56% of White smokers but only 32% of Black smokers. If the narrow criteria are applied to the never-smokers, the disparity is complete. The never-smokers are invisible to the early detection mechanisms, which would have made them candidates for the therapies that were demonstrated in the IPASS study. 

Furthermore, there is a tremendous disparity in the tests that are administered in the “precision medicine” age. Due to environmental or economic reasons, a Black or Hispanic individual is far less likely to receive the necessary molecular diagnostic tests that are necessary for the administration of lifesaving TKIs. Without this data, physicians are forced to resort to the traditional platinum-based chemotherapy, which may result in an inferior outcome depending on the cancer cause. This leads to a problem that is unclear whether the treatment was simply ineffective or if the individual was just diagnosed too late to benefit. 

Proposal For a New Form of Treatment

This paper proposes a new targeted form of treatment for ethnic minorities. This treatment would target the specific mutations that make particular ethnic groups more susceptible to NSCLC. The aim is to help reduce suffering and the progression of NSCLC in ethnic minority groups. 

Previous research in East Asian groups who have advanced NSCLC and have EGFR activating mutations has shown that treatments such as gefitinib, erlotinib and afatinib are effective in terms of improving a patient’s objective response rate and progression-free survival (Zhou & Zhou, 2018). Studies also show improved tolerability in patients in comparison to standard platinum-based double chemotherapy (Fukuoka et al., 2011). EGFR-TKI treatment has been the most effective for treating lung adenocarcinomas in East Asian never-smokers (Wu et al., 2014; Mok et al., 2009; Nan et al., 2017). The essential part of this treatment is that it works by inhibiting tyrosine kinase signalling to temporarily or permanently prevent signals from being sent from one cell to another. As the tyrosine kinase acts as receptors for these signals on cells, blocking cancerous cells from sending signals to healthy cells reduces the rate of metastasis. This prevents uncontrolled cell proliferation caused by overactive EGFR signaling, which can cause cancer (Fukuoka et al., 2011). We can utilise the way this treatment works to aid in the intervention and treatment of NSCLC in ethnic minorities.

This paper proposes a more inclusive and universal treatment to more accurately identify LCINS in ethnic minorities. Furthermore, by making clinical trials more representative using, for example, stratified sampling to get an accurate representation of the disparity of different racial groups in the population, it will allow for a more generalisable treatment to be pushed forward. The treatment will first utilise lung screening trials of each underrepresented ethnic minority group (Black, East Asian, Hispanic) never-smokers to help accurately identify cases of lung cancer. By utilising low-dosage helical computed tomography to obtain a multiple-image scan of the entire chest and a standard chest X-ray, we can help to provide early detection through screening (UC Health, 2021). 

By using computed tomography for a diagnosis, patients can then receive molecular diagnostic tests, which would study their DNA, RNA and proteins in a fluid/tissue sample which can be received from their lung (CancerGov, 2024). This will allow for the further identification of the type of mutation that the patient may be experiencing: ALK and ROS1-oncogenic drivers, causing cells to proliferate uncontrollably; EGFR mutations, the most common type of mutation associated with lung cancer in never-smokers (de Alencar et al., 2022); or KRAS, which, when mutated, can become stuck in the “on” position, causing cells to proliferate uncontrollably and metastasise (Chien, 2021).

In addition to molecular testing, this paper proposes the use of AI to help accurately identify which mutations may have occurred. By analysing high-quality biopsies and helping to identify how far along the mutation may be, AI can help to scale the severity of the mutation and aid in deciding which form of treatment will have the most beneficial impact on the mutated gene. It can also allow for the production of higher quality 3D images of the mutated genes by analysing raw DNA sequences and chromatin accessibility data to learn how genes are likely arranged based on their underlying sequence, allowing for more precise pin pointing of the mutation (Zhang, 2009). Furthermore, prior studies have utilised AI to help extract additional information about the chemical composition of lung tumours from medical scans (Welch, 2025; Aboagye et al., 2024). This is a non-invasive method which has proved effective in selecting the right treatment for patients (Welch, 2025). 

The usage of molecular diagnostic tests can allow us to further separate patients based on the treatment they will need. If there is a mutation in the EGFR gene, we can then utilise the benefits of the EGFR-TKI treatment to help target the mutation of the EGFR gene specifically as opposed to a form of treatment which will generally attack a range of genes. However, due to the lack of evidence upon the effect in which this treatment may have on Black patients, we will have to monitor the symptoms of each generation of the EGFR-TKI treatment to see if there are any unwanted side effects. While side effects are expected to be minimal, ongoing monitoring is necessary.

The benefits of target gene inhibitors after platinum-based chemotherapy and immunotherapy are typically the first line of treatment for a KRAS mutation (Aboagye et al., 2024); however, this is based on unrepresentative data. We are therefore also proposing the testing of platinum-based therapy and immunotherapy on the ethnic minority groups East Asian, Black and Hispanic to evaluate its potency within these groups. If that first line of treatment does prove to be effective, the next stages of our treatment, which consists of the usage of targeted inhibitors for these genes either as a second or first line of treatment, will be used. However, the usage of platinum-based chemotherapy and immunotherapy will also need to be closely monitored. AI can be utilised here for constant monitoring and data recording of tumour progression or regression. 

Finally, treatment will mainly focus on and prioritise ethnic minorities who live in areas which have environmental factors that pose a high risk of lung cancer in never-smokers. By targeting people who fall under this category first, it will allow for early detection of lung cancer adenocarcinomas, allowing for less vigorous and invasive treatment to be needed.

Conclusion

In conclusion, there are numerous factors that contribute to the increased likelihood of lung cancer in never-smokers in ethnic minorities, such as increased likelihood of genetic mutation and novel variants (Shen et al., 2012). In addition, specific traditions and cultural practices, such as incense burning or the use of high cooking temperatures in East Asian cultures, can emit fumes that are high in polycyclic aromatic hydrocarbons (Kim, 2015; Cheng, 2021). Additionally, Black populations have been found to experience higher occupational exposure to carcinogens due to disproportionate employment in manual work industries (United States Environmental Protection Agency, 2021; Dillard, 2023; Lancaster University, 2021). Although this has been recognised, there has been minimal progress made in addressing this.

Therefore, this paper suggests a way to close the gap of disparity between minorities and the majority with our newly proposed approach to treatment of NSCLC in ethnic minorities. Our newly proposed treatment aims to reduce the progression and risk of undetected NSCLC in ethnic minorities, allowing for early detection and intervention.

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