Skip to main content

Understanding exposomes and its relation with cancer risk in Malaysia based on epidemiological evidence: a narrative review


The prevalence of cancer is increasing globally, and Malaysia is no exception. The exposome represents a paradigm shift in cancer research, emphasizing the importance of a holistic approach that considers the cumulative effect of diverse exposures encountered throughout life. The exposures include dietary factors, air and water pollutants, occupational hazards, lifestyle choices, infectious agents and social determinants of health. The exposome concept acknowledges that each individual’s cancer risk is shaped by not only their genetic makeup but also their unique life experiences and environmental interactions. This comprehensive review was conducted by systematically searching scientific databases such as PubMed, Scopus and Google Scholar, by using the keywords “exposomes (environmental exposures AND/OR physical exposures AND/OR chemical exposures) AND cancer risk AND Malaysia”, for relevant articles published between 2010 and 2023. Articles addressing the relationship between exposomes and cancer risk in the Malaysian population were critically evaluated and summarized. This review aims to provide an update on the epidemiological evidence linking exposomes with cancer risk in Malaysia. This review will provide an update for current findings and research in Malaysia related to identified exposomes-omics interaction and gap in research area related to the subject matter. Understanding the interplay between complex exposomes and carcinogenesis holds the potential to unveil novel preventive strategies that may be beneficial for public health.


Understanding exposomes and its relation with carcinogenesis

Cancer is known for its multifactorial etiology and a complex disease continues to be a leading cause of death worldwide. While genetic factors have long been recognized as important contributors to cancer risk, emerging research has shed light on the significant influence of environmental exposures. One field in epidemiology that greatly relies on improved measurements is exposure assessment, and this need has been emphasized through the concept of the exposome. Moreover, the ability to observe genetic and epigenetic changes in individuals exposed to potential risk factors offers an opportunity to understand the underlying mechanisms of cancer development, leading to earlier detection and more precise categorization of the disease at a molecular level.

The exposome signifies a comprehensive assessment of all lifelong environmental influences (including biological, chemical, physical, and psychosocial factors) and the corresponding biological reactions within an individual, in addition to the pre-existing genetic factors. The discussion about exposomes normally will involve 3 different aspects which include internal exposomes (metabolism, endogenous circulating hormones, body morphology, physical activity, gut microbiota, inflammation, etc.), external exposures (radiation, infections, chemical contaminants and pollutants, diet, lifestyle factors, occupational hazards) and lastly general external exposures (social and psychological influences on the individual which also include natural build environment) [1]. Figure 1 illustrates exposomic framework that include external exposure such as lifestyle, environment and social that will influence cancer risk through changes in the multi-omics markers indicated in the diagram. Although it looked very complex but identifying risk factors by combining whole exposomic framework is beneficial for policymakers and stakeholder to formulate best cancer prevention strategies for public health.

Fig. 1
figure 1

Exposomic approach and carcinogenesis

In a pioneering study involving the sequencing of the entire tumor genome, researchers focused on a small cell lung cancer (SCLC) cell line, comparing it with genomic DNA obtained from an Epstein-Barr virus-transformed lymphoblastoid line from the same patient. The analysis unveiled more than 20,000 somatic single nucleotide variants (point mutations) [2]. Strong association between SCLC and smoking, along with the prevalence of G to T transversions as induced by oxidative stress via formation of 8-hydroxy-2-deoxyguanosine (8-OHdG), and other mutations typically associated with tobacco exposure, supported the hypothesis that this mutation spectrum represented the signature of tobacco influence across the cancer’s entire genome. In a separate report by Pleasance et al. [2010] [3], a similar approach was used to investigate mutations in a melanoma cell line. The mutational pattern in this case indicated a significant influence of sunlight, aligning with earlier data on TP53 mutation spectra.

An illustrative instance is evident in head and neck cancers, which exhibit strong connections to prior tobacco and alcohol exposure. Additionally, particularly in high-income countries, these cancers are associated with mucosal human papilloma viruses (HPV) infection. Stransky et al. conducted whole-exome sequencing on 74 tumors, revealing that HPV-positive tumors had approximately half the mutation rate compared to HPV-negative tumors, although with an overall 40-fold variation. G to T transversion mutations were prevalent, and tumors with a higher fraction of G to T mutations had more mutations in total, suggesting a general effect of tobacco mutagens [4].

Using a similar exome-sequencing approach, Agrawal et al. studied 32 tumors and found an average of 19 mutations per tumor, with a range of 2–78 [5]. Again, there were fewer mutations in HPV-associated tumors and, on average, about twice as many in tumors from tobacco users. However, unlike Stransky et al.‘s study [4], there was no enrichment for G to T transversions in this series. This could be attributed to the inclusion of a significant proportion of laryngeal tumors in Stransky et al.‘s larger study, which are less likely to be linked to HPV infection and thus exhibit higher mutation rates and G to T transversion frequencies than tumors from other sites.

Besides whole genome sequencing, exposomic study can also be identified using other biomarkers such as metabolites, gene expression changes, metagenomics and other omics approach. Combining those multi-omics approach will provide a more precise outcome in terms of providing algorithm for prediction or prognosis of disease. EPIC (European Prospective Investigation into Cancer and Nutrition) is one of the best cohorts that employs similar method and yield best outcome to understand etiology of cancer in Europe [67].

The application of metabolic fingerprinting analytical techniques allows us to examine the distinctive set of metabolites present in biological samples that involved in various pathophysiological processes of a disease, with a focus on cancer in the present context. However, very few studies related to metabolomics and cancer risk was conducted in Malaysia. One recently published study revealed that the metabolite profile associated with colorectal cancer (CRC) cases in Malaysia were hypoxanthine, acetylcarnitine, xanthine, uric acid, tyrosine, methionine, lysoPC, lysoPE, citric acid, 5-oxoproline, and pipercolic acid. The data also showed that the most perturbed pathways in CRC were purine, catecholamine, and amino acid metabolisms [8].

The application of exposome framework can be seen now not only in cancer studies [9,10,11] but also in other non-communicable diseases such as cardiovascular disease [12,13,14] and respiratory disease [15,16,17]. A study by Juarez et al. [18], used an exposome database containing more than 2000 environmental exposures from natural, built and social environment domains and they observed that exposure to ethylene oxide and ethyl dichloride, particulate matter (PM)2.5 and cigarette closely associated with lung cancer. Another study focusing on skin cancer suggested that physico-chemical substances, living organisms (viruses) and lifestyle factors made up exposome for this cancer [19]. A study on pancreatic cancer suggested that several exposome factors were related to pancreatic cancer alone and in combination with other exposures [20]. A recent study by Chen et al. reported that lifestyle, social and ecosystem domains are related to CRC events and incidence [21].

The study involving exposomes normally will involve big data analysis from a cohort study and multiple biomarkers. Lack of cohort study conducted in Malaysia may be one of the limitations in obtaining published evidence related to exposomes and cancer risk. Nevertheless, this field of research is still emerging and very limited epidemiological evidence reported in Malaysian setting especially focusing on cancer risk. To date, no study on whole exposomes and cancer risk has been conducted in Malaysia. Most of the studies reported are conducted individually according to the risk factors and not combining the whole exposome approach. This review will summarize studies published in this area and will identify research gap for other researchers to take opportunity and contribute to the body of knowledge.

Main text

Environmental exposure and cancer risk in Malaysia

The study about environmental contaminants in Malaysia is normally being conducted not in a cohort setting. Most researchers would conduct a cross-sectional study design and experimental design study where they would study contaminants in the identified source. However, there are few studies conducted on air pollution studied the impact of particulate matter with lung cancer risk.

A study by Othman et al. [22] in school classroom in Kuala Lumpur suggested that the major source of indoor dust was road dust (69%), while soil dominated the outdoor dust (74%). Health risk assessment conducted showed that the hazard quotient (HQ) value for non-carcinogenic trace metals was < 1 while the total cancer risk (CR) value for carcinogenic elements was below the acceptable limit (1.0E-06–1.0E-04) for both indoor and outdoor dust through dermal and inhalation pathways, but not the ingestion pathway. This study suggests indoor contributions of PM2.5 concentrations are due to the activities of the school children while the compositions of indoor and outdoor dust are greatly influenced by the soil/earth source plus industrial and traffic contribution. The major ion and trace metal concentrations in indoor and outdoor dust were Al, Fe, Zn, V, Cu and Ca2+ while for outdoor dominant elements and ions were Al, Fe, Zn, SO42−, Ca2+ and V. Most of the studies in Malaysia conducted is via this way which is not from epidemiological evidence. However, it is worth to note that the study conducted is still important and provide preliminary data on exposure assessment.

Another study conducted from the same group in office environment showed the higher total CR value for outdoors (2.67E-03) was observed compared to indoors (4.95E-04) under chronic exposure, thus suggesting a carcinogenic PM2.5 risk for both the indoor and outdoor environments [23]. It was noted that the CR value reported in this study was estimated based on the inhalation unit risk (IUR), where the CR was calculated by multiplying the exposure concentration by the IUR (standard value of unit risk of 0.008 per µg m− 3).

A study by Sopian et al. (2021) [24] investigated the association of exposure to particle-bound (PM2.5) polycyclic aromatic hydrocarbons (PAHs) with potential genotoxicity and cancer risk among children living near the petrochemical industry and comparative populations in Malaysia. They collected PM2.5 samples using a low-volume sampler for 24 h at three primary schools located within 5 km of the industrial area and three comparative schools more than 20 km away from any industrial activity. A total of 205 children were randomly selected to assess the DNA damage in buccal cells. This study revealed that the inhalation risk for the exposed children and comparative populations was 2.22 × 10− 6 and 2.95 × 10− 7, respectively, based on the 95th percentiles of the incremental lifetime cancer risk estimated using Monte Carlo simulation [24]. The degree of DNA injury was substantially more severe among the exposed children relative to the comparative community, hence indicating that higher exposure to PAHs increases the risk of genotoxic effects and cancer among children.

Another study conducted in Rawang, Malaysia showed that the highest potentially toxic element concentration was Pb (593.3 mg/kg), whereas the lowest was Co (5.6 mg/kg) [25]. Potentially toxic elements (Cu, Cd, Pb, Zn, Ni and Cr) were linked with anthropogenic sources (urbanization process, industrial and commercial growth, urban traffic congestion). Non-carcinogenic risk by hazard index (HI) value more than 1.0 was indicated for adults and children. Similarly, carcinogenic risk by total lifetime cancer risk value also showed carcinogenic risks among adults and children.

In another study recently published [26], indoor dust is an important medium to evaluate human exposure to emerging organic contaminants. The dominant chemical groups of organic micropollutants (OMPs) of indoor dust were ascribed to n-alkanes (median: 274 µg/g), plasticizers (151 µg/g), sterols (120 µg/g), and pesticides (42.6 µg/g). The cancer risks of all OMPs were greater than 10− 4. This study offers a benchmark to show exposure assessment of chemicals in Malaysia.

A study was also conducted to investigate heavy metal contamination in paddy plants as this is our staple food in our country both in northern and eastern region. The health risk assessment was performed based on United States Environmental Protection Agency (USEPA) guidelines. The enrichment factor for heavy metals in the studied areas was in the descending order of Cu > As > Cr > Cd > Pb. Meanwhile, Cr and Pb exhibited higher translocation values from stem to grain compared with the others. The combined HI resulting from five heavy metals exceeded the acceptable limit (HI > 1). The lifetime CR, in both adult and children, was beyond the acceptable limit (10− 4) and mainly resulted from exposure. The total CR due to simultaneous exposures to multiple carcinogenic elements also exceeded 10− 4. It was concluded that the intake of heavy metal through rice ingestion is likely to cause both non-carcinogenic and carcinogenic health risks [2728].

Another study conducted in 2019 [29] identified risk factors associated with lung cancer diagnosis and death by using epidemiological evidence. Lung adenocarcinoma was diagnosed in predominantly younger, female non-smokers compared to the other types of lung cancers. Lung adenocarcinoma subjects had annual PM2.5 that was almost twice higher than squamous cell carcinoma, small cell carcinoma and other histological subtypes. The high-risk cluster was characterized by occupational exposure to air pollution for over four hours daily, reliance on motorcycles and trucks for transportation, and a mean annual PM2.5 concentration. Individuals in the high-risk cluster exhibited more than five times higher risk for being diagnosed with lung adenocarcinoma (OR = 5.69, 95% CI = 3.14–7.21, p < 0.001) and a hazard ratio (HR) of 3.89 (95% CI = 2.12–4.56, p = 0.02) for lung adenocarcinoma mortality at one year. This is the only study that associated environmental exposure with risk of cancer in Malaysia based on epidemiological evidence.

Dietary carcinogens and cancer risk in Malaysia

Publications from Malaysia were reviewed regarding various food components such as N-nitroso compounds, PAHs, and heterocyclic aromatic amines (HAAs), that have been identified as human carcinogens by the International Agency for Research on Cancer (IARC). Some other possible carcinogenic agents are also considered in this review, such as acrylamide and salted or other preserved foods which are common in Malaysian diet.

Carcinogenic nitrosamines, specifically N-nitrosodimethylamine (NDMA), N-nitrosodiethylamine, N-nitrosodibutylamine, N-nitrosopyrrolidine, and N-nitrospiperidine, are formed during the curing of meats with nitrite [30]. These nitrosamines undergo metabolic activation in the gastrointestinal tract by cytochrome P450 2E1. NDMA, in particular, generates a reactive intermediate that leads to the formation of DNA adducts, such as N7-methyl-2′-deoxyguanosine (N7-MedG), resulting in abasic site formation, DNA strand breaks, and cytotoxicity. Another DNA adduct is formed through O6-methylation of deoxyguanosine (dG), leading to O6-methyl-2′-deoxyguanosine (O6-MedG). Additionally, an endogenously formed nitrosated glycine from the consumption of red meat may induce specific mutations, such as G-A transitions and G-T transversions, in genes that promote cancer, including H-Ras and K-Ras oncogenes, as well as the p53 tumor suppressor gene [31].

Despite the increasing consumption of red meat as part of the nutrition transition in Asia, there is a notable lack of research in this area, creating a substantial research gap. No direct study has linked N-nitroso compound with cancer risk in Malaysia based on epidemiological evidence.

Next to be discussed is PAHs, which can originate from different sources, such as air PM and the combustion of organic material found in food. Procarcinogens like PAHs do not directly cause genotoxicity; instead, they need to undergo metabolic transformations into more reactive metabolites through xenobiotic-metabolizing enzymes, such as cytochrome P450 (CYP) 1A1/1B1, epoxide hydrolase, and aldo-keto reductase. These transformations lead to the formation of phenols, catechols, quinones, diol-epoxides, o-quinones, and radical cations [32], which can react with DNA and form DNA adducts. The risk of carcinogenesis is determined by both the level of DNA damage and the capacity to repair the damage. Carcinogenic PAHs can induce DNA damage in various human cell lines, triggering downstream DNA damage response gene products that regulate and maintain genomic stability [33]. Research exploring the association between PAHs exposure and cancer risk has been extensively conducted in China. These studies assessed the proportion of dietary intake relative to total PAHs intake and examined the correlation between dietary PAHs intake and the occurrence of abnormal lung cancer cases [34,35,36]. No other studies has been reported in Malaysia even related to food groups that may be associated with PAHs and cancer risk.

HAAs, which include 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx), and 2-amino-9H-pyrido[2,3-b]indole (AαC), are highly prevalent in well-done cooked meats [37]. These compounds are activation-dependent and are formed through heat-induced reactions primarily found in foods containing nitrogenous and creatine components. The quantity of HAAs is influenced by cooking temperature and the intensity of heat applied during the cooking process. HAAs can cause single strand breaks in DNA, chromosomal aberrations, and DNA adducts in guanine-rich regions. Activated metabolites can attach to DNA at the N2-position of guanine (more common) or the C8-atom of guanine (less frequent) [38]. White meat generally contains lower levels of HAAs, likely due to reduced cooking time. Another factor that may influence HAAs in white meat is the use of marinades, as different types of marinades used with chicken have been shown to impact HAAs production [39].

In terms of mechanism, HAAs undergo metabolism by cytochrome P450 enzymes, resulting in the formation of genotoxic N-hydroxylated metabolites. These metabolites then undergo further metabolism with conjugation enzymes, such as N-acetyltransferases or sulfotransferases, leading to the generation of reactive intermediates that bind to DNA, causing genomic instability that may be one of the key factors of carcinogenesis. In Malaysia, fried and grilled chicken was found to be the major dietary source of HAAs [40].

For acrylamide, the genotoxic properties of acrylamide suggest that it could potentially contribute to neoplastic transformation. The carcinogenic potential of acrylamide was demonstrated in the studies conducted by Friedman et al. in 1995. These studies revealed a notable rise in the occurrence of thyroid follicular cell adenomas and adenocarcinomas in male rats, as well as a significant increase in mammary gland fibroadenoma and adenocarcinomas in female rats [41].

In one of the studies, biomarkers of acrylamide and dietary estimates were examined, and it was observed that the consumption of crackers and chocolate showed a significant association with the concentrations of a major metabolite of acrylamide, namely N-acetyl-S-(2-carbamoylethyl)-cysteine (AAMA), in urine [42]. A large cohort study in Japan is the only study investigated on dietary acrylamide and risk in breast, gastric, lung, pancreatic, liver, colorectal, endometrial, and ovarian cancer. However, no significant association was found between dietary acrylamide and the risk of any of these types of cancer [43,44,45,46,47]. Perhaps Malaysian researcher should learn from the Japanese cohort to link their public cohort with dietary carcinogen. Such valuable data is really critical for public health strategies and policy making for years to come.

Notably, Hogervorst et al. [48] made an interesting discovery, demonstrating a significant correlation between dietary acrylamide intake and specific single-nucleotide polymorphisms (SNPs) in acrylamide-metabolizing enzymes, such as cytochrome P450 2E1, concerning the risk of endometrial cancer. Furthermore, they found a notable interaction between SNPs in the HSD3B1/B2 gene cluster, which affects progesterone or androgens, related to the risk of ovarian cancer.

Dietary acrylamide may also raise the risk of cutaneous malignant melanoma in men (HR: 1.13, 95% CI: 1.01–1.26) per 10 µg increment, and risk of lymphatic malignancies, such as multiple myeloma and follicular lymphoma, in men [4950]. A very recent study published in Japan showed that dietary acrylamide has an association with risk of breast cancer through its effect on haemoglobin adducts [51]. It is known that acrylamide causes cancer owing to its mutagenic and genotoxic metabolite, glycidamide, and its effects on sex hormones. Both acrylamide and glycidamide can interact with hemoglobin to hemoglobin adducts, which may be one of the key features of cancer hallmarks.

In Malaysia, the only risk assessment study of dietary acrylamide reported is by Sharif et al. 2018 that was conducted in university students [52]. The students’ intake of coated fried chicken can give a significant health risk compared to other tested food, and all of the tested food sold in the canteen give a high number of probabilities of increased risk of cancer.

Besides known dietary carcinogen, it is worth to note on food groups and cancer risk. Limited data representing Malaysia in this field of research making this review very short. In one of the recently published case-control study, pro-inflammatory diets which contains foods that may potentially promote inflammation within the body, such as food high in sugar, refined flour, saturated fats, and red and processed meats, were reported to be associated with an increased incidence of colorectal cancer in the Malaysian population, particularly in obese subjects [53]. From the same cohort of subjects, four main dietary patterns were identified: the allergenic diet, plant-based diet, processed diet, and energy-dense diet pattern. After adjusting for potential covariates, the processed diet pattern was consistently associated with CRC (OR = 3.45; 95% CI = 1.25–9.52; P = 0.017) while the plant-based diet, energy-dense diet, and allergenic diet were not associated with CRC risk [54]. Another study to associate dietary pattern with colorectal adenoma risk showed that red meat consumption showed a positive association [55].

Another important evidence to note based on Malaysian landscape is related to nasopharyngeal carcinoma (NPC). Since the 1980-s, evidence on consumption of salted food with NPC were reported [56,57,58,59]. It was postulated that salt can help in the nitrosation process and may produce dangerous oncometabolites, as well as being involved in promoting Epstein Barr virus, which is a common feature in those with NPC. In an in vitro toxicity model, salt and nitroso compounds were identified as inducers of mutagenicity and genome damage [6061]. The cancer incidence also may be related to the genetic polymorphism, Epstein-Barr virus and many other confounding factors that should be included in the risk factors by using the exposome model framework which warrants further investigation in this area of research.

Top of form

Occupational hazards and cancer risk in Malaysia

Malaysia’s diverse economy encompasses various industries, some of which expose workers to potential carcinogens such as asbestos, solvents, and heavy metals. Workers in these industries may face elevated cancer risks related to their specific occupational exposures.

To date, there is no direct study reported on occupational hazard and exposure with cancer risk or any cancer hallmarks. However, there is one study related to exposure of radiation in tin by-product processing industry workers reported in Malaysia [62]. With poorly established safety and health practices in operating plant, amang poses extremely high radioactivity problem associated with high occupational ionizing radiation exposures to workers. The study found out that for 8 h of work time, a worker is estimated to receive an average effective dose of 0.1 mSv per day from external γ radiation source with a maximum up to 2 mSv per day for extreme exposure situation.

Interferences of different exposure routes for examples inhalation of equivalent equilibrium concentration (ECC) of 222Rn and 220Rn progenies and airborne long-lived α particles from the dusty working environment could pose a higher total effective dose as much as 5 mSv per day and 115 mSv per year. The value is 5 times higher than the annual dose limit for designated radiation worker (20 mSv) in Peninsular Malaysia. The study found that 41% of the total received an effective dose received by a worker was contributed by 222Rn, 32% of airborne particulates and dust, 23% from external γ exposure and 4% from 220Rn. This rare earth element is a known genotoxic agent and may contribute to one of the key components in cancer hallmarks which is genomic stability.

Further findings from Malaysia investigated genetic damage due to occupational exposure in auto repair workshop workers. Micronucleus frequency, comet tail length and relative telomere length differences were significantly greater in the auto repair workshop workers. Duration of working time was significantly associated with micronucleus frequency, comet tail length and relative telomere length [63]. Another study investigating workers and genotoxic effects revealed that paddy farmers who chronically exposure to a mixture of organophosphates has at least 2-fold significant increase of DNA damage as compared with control group [64].

Lack of data in this focus area warrants further investigation as occupational hazard and exposure are one of the main exposures for cancer carcinogenesis.

Infectious agents and cancer risk in Malaysia

Certain infections, such as Helicobacter pylori (linked to stomach cancer) and the HPV (linked to cervical and other cancers) infections, represent significant cancer risk factors in Malaysia.

Based on published evidence, it has been shown that Helicobacter pylori may be associated with the increased risk of gastric cancer, particularly in relation to high salted food consumption by Malaysian population [65].

In Malaysia, cervical cancer is the third leading cause of female cancer deaths and the second most common cancer that occurs in women aged 15 to 44 years old with 621 deaths annually [66]. HPV are small non-enveloped viruses, with a double-stranded circular DNA genome. This virus is oncogenic and caused persistent infection in the human system, hence leading to carcinogenesis. The two most important proteins in the carcinogenesis of cervical cancer are E6 and E7, which are responsible for the dysregulation of the cell cycle [67]. A study by Rahmat et al. 2021 showed that the most common high-risk HPV type among women living in urban areas in Malaysia is HPV 52, which is not the type of infection the current HPV vaccine is covered for protection among females [68]. This data is very important because it might evidence to the stakeholders on why cervical cancers is still increasing in Malaysia despite the vaccines given.

Socioeconomic factors and cancer risk in Malaysia

Disparities in socioeconomic status and access to healthcare can influence cancer risk and outcomes. Low socioeconomic status may lead to increased exposure to environmental carcinogens and limited access to early detection and treatment services. Despite looking thoroughly on socioeconomic factors and cancer risk in Malaysia, only one study reported on HPV infection which reflects cervical cancer that was significantly associated with employment (OR 4.94; CI 1.58–15.40) and education at secondary/high school level [69]. Only few studies have focused on the influence of social determinants on the risk of cancer. Hastert et al. used data from the Vitamins and Lifestyle Study to examine the relationship between socioeconomic status and CRC incidence. Living in the lowest socioeconomic status areas was associated with a higher CRC incidence than those living in the higher socioeconomic status areas [70]. This can be due to the access of medical facility.

A comprehensive review by Carethers and Doubeni in 2020 showed that a disadvantaged socioeconomic position is related to an increased risk of CRC [71]. Social support was another social factor that affected colorectal cancer carcinogenesis where lower social support was associated with a higher incidence of CRC [71]. Additionally, social support reduces stress and depression. Social support raises the esteem of individuals and makes them feel valued; therefore, they may take better care of themselves and be more receptive to preventative services. They also may experience lesser stress hormones to reduce the risk of immune dysregulation, thereby suppressing the environment for tumour initiation.

It is obvious that in Malaysia, social and economic factors should be included in any of the exposure assessment related to health impact in this case carcinogenesis. Perhaps it is due time that we relook again at how we design our study to incorporate all of the exposomes.


Designing exposomic framework to understand cancer carcinogenesis is really critical and important to understand. As listed in this review, there is a huge gap in epidemiological evidence in relation to any omics marker and cancer risk integrated with any of the exposomes, especially in Malaysia. Figure 2 illustrates exposomic map of Malaysian data based on cancer risk published. This creates research gap for Malaysian researchers and promote global collaborations with other researchers.

Fig. 2
figure 2

Mapping exposomes and cancer risk in Malaysian landscape

This review is of course with a lot of limitation due to limited data published in Malaysia. Perhaps this article will assist to shed lights to cancer and toxicology researchers who wants to understand the complex interplay between environmental-lifestyle and carcinogenesis. Nevertheless, understanding the exposome and its relation to cancer risk in Malaysia is of paramount importance for several reasons:

  1. 1.

    Unique Exposures: Malaysia’s population is exposed to a distinctive set of environmental factors, lifestyle choices, and dietary habits that may differ from other regions. Investigating the specific exposome in Malaysia can uncover novel carcinogens and risk factors that are relevant to the local population.

  2. 2.

    High Cancer Burden: Cancer is a significant public health concern in Malaysia, with a substantial number of cancer cases diagnosed each year and present huge socioeconomic burden for Malaysian government. Identifying the key environmental and lifestyle factors contributing to cancer risk can help implement targeted preventive measures and interventions to reduce the cancer burden.

  3. 3.

    Prevention Strategies: By comprehensively studying the exposome and its link to cancer risk, policymakers and healthcare professionals can develop effective preventive strategies tailored to the Malaysian population. This may include awareness campaigns, lifestyle modifications, and environmental regulations to minimize cancer risk factors.

  4. 4.

    Precision Medicine: Understanding the exposome’s impact on cancer risk can enable personalized approaches to cancer prevention and treatment. By considering individual variations in exposure, genetics, and lifestyle, healthcare providers can offer more targeted and effective interventions.

  5. 5.

    Environmental Sustainability: Research on the exposome can also shed light on environmental hazards and pollution that may contribute to cancer risk. Addressing these issues can promote environmental sustainability and protect both human health and the ecosystem. It is critical time for all the stakeholders and ministries to work together for this purpose.

  6. 6.

    Global Research Collaboration: Studying the exposome and cancer risk in Malaysia contributes to the broader global effort to understand cancer etiology. Collaborative research can lead to shared knowledge and strategies for cancer prevention and control worldwide.

Overall, investigating the exposome and its relation to cancer risk in Malaysia is essential for improving public health, reducing cancer incidence, and advancing cancer research and prevention strategies in the region and beyond.

Data availability

Not applicable.


  1. Münzel T, Sørensen M, Hahad O, Nieuwenhuijsen M, Daiber A. The contribution of the exposome to the burden of cardiovascular disease. Nat Rev Cardiol. 2023 May;10.

  2. Pleasance ED, Cheetham RK, Stephens PJ, McBride DJ, Humphray SJ, Greenman CD, Varela I, Lin ML, Ordonez GR, Bignell GR, Ye K, Alipaz J, Bauer MJ, Beare D, Butler A, Carter RJ, Chen L, Cox AJ, Edkins S, Kokko-Gonzales PI, Gormley NA, Grocock RJ, Haudenschild CD, Hims MM, James T, Jia M, Kingsbury Z, Leroy C, Marshall J, Menzies A, Mudie LJ, Ning Z, Royce T, Schulz-Trieglaff OB, Spiridou A, Stebbings LA, Szajkowski L, Teague J, Williamson D, Chin L, Ross MT, Campbell PJ, Bentley DR, Futreal PA, Stratton MR. A comprehensive catalogue of somatic mutations from a human cancer genome. Nature. 2010;463:191–6.

    Article  ADS  CAS  PubMed  Google Scholar 

  3. Pleasance ED, Stephens PJ, O’Meara S, McBride DJ, Meynert A, Jones D, Lin ML, Beare D, Lau KW, Greenman C, Varela I, Nik-Zainal S, Davies HR, Ordonez GR, Mudie LJ, Latimer C, Edkins S, Stebbings L, Chen L, Jia M, Leroy C, Marshall J, Menzies A, Butler A, Teague JW, Mangion J, Sun YA, McLaughlin SF, Peckham HE, Tsung EF, Costa GL, Lee CC, Minna JD, Gazdar A, Birney E, Rhodes MD, McKernan KJ, Stratton MR, Futreal PA, Campbell PJ. A small-cell lung cancer genome with complex signatures of tobacco exposure. Nature. 2010;463:184–90.

    Article  ADS  CAS  PubMed  Google Scholar 

  4. Stransky N, Egloff AM, Tward AD, Kostic AD, Cibulskis K, Sivachenko A, Kryukov GV, Lawrence MS, Sougnez C, McKenna A, Shefler E, Ramos AH, Stojanov P, Carter SL, Voet D, Cortes ML, Auclair D, Berger MF, Saksena G, Guiducci C, Onofrio RC, Parkin M, Romkes M, Weissfeld JL, Seethala RR, Wang L, Rangel-Escareno C, Fernandez-Lopez JC, Hidalgo-Miranda A, Melendez-Zajgla J, Winckler W, Ardlie K, Gabriel SB, Meyerson M, Lander ES, Getz G, Golub TR, Garraway LA, Grandis JR. The mutational landscape of head and neck squamous cell carcinoma. Science. 2011;333:1157–60.

    Article  ADS  CAS  PubMed  PubMed Central  Google Scholar 

  5. Agrawal N, Frederick MJ, Pickering CR, Bettegowda C, Chang K, Li RJ, Fakhry C, Xie TX, Zhang J, Wang J, Zhang N, El-Naggar AK, Jasser SA, Weinstein JN, Trevino L, Drummond JA, Muzny DM, Wu Y, Wood LD, Hruban RH, Westra WH, Koch WM, Califano JA, Gibbs RA, Sidransky D, Vogelstein B, Velculescu VE, Papadopoulos N, Wheeler DA, Kinzler KW, Myers JN. Exome sequencing of head and neck squamous cell carcinoma reveals inactivating mutations in NOTCH1. Science. 2011;333:1154–7.

    Article  ADS  CAS  PubMed  PubMed Central  Google Scholar 

  6. Braillon A. European prospective investigation into Cancer and Nutrition (EPIC): methods and clinical relevance. Am J Clin Nutr. 2011;93(6):1386–7. author reply 1387-8.

    Article  CAS  PubMed  Google Scholar 

  7. Margetts BM, Pietinen P. European Prospective Investigation into Cancer and Nutrition: validity studies on dietary assessment methods. Int J Epidemiol. 1997;26 Suppl 1:S1-5. PMID: 9126528.

  8. Amir Hashim NA, Ab-Rahim S, Wan Ngah WZ, Nathan S, Ab Mutalib NS, Sagap I, Jamal A, Mazlan AR. Global metabolomics profiling of colorectal cancer in Malaysian patients. Bioimpacts. 2021;11(1):33–43.

    Article  PubMed  Google Scholar 

  9. Zhu AY, McWilliams TL, McKeon TP, Vachani A, Penning TM, Hwang WT. Association of multi-criteria derived air toxics hazard score with lung cancer incidence in a major metropolitan area. Front Public Health. 2023;11:1002597.

    Article  PubMed  PubMed Central  Google Scholar 

  10. Go YM, Weinberg J, Teeny S, Cirillo P, Krigbaum N, Singer G, Ly V, Cohn B, Jones DP. Exposome Epidemiology for Suspect Environmental Chemical Exposures during pregnancy linked to subsequent breast Cancer diagnosis. medRxiv [Preprint]. 2023 Jun 27:2023.06.20.23291648.

  11. Krieger KL, Mann EK, Lee KJ, Bolterstein E, Jebakumar D, Ittmann MM, Dal Zotto VL, Shaban M, Sreekumar A, Gassman NR. Spatial mapping of the DNA adducts in cancer. DNA Repair (Amst). 2023;128:103529.

    Article  CAS  PubMed  Google Scholar 

  12. Bonanni A, Basile M, Montone RA, Crea F. Impact of the exposome on cardiovascular disease. Eur Heart J Suppl. 2023;25(Suppl B):B60–4.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  13. Lee EY, Akhtari F, House JS, Simpson RJ Jr, Schmitt CP, Fargo DC, Schurman SH, Hall JE, Motsinger-Reif AA. Questionnaire-based exposome-wide association studies (ExWAS) reveal expected and novel risk factors associated with cardiovascular outcomes in the personalized environment and genes study. Environ Res. 2022;212(Pt D):113463.

    Article  CAS  PubMed  Google Scholar 

  14. Poveda A, Pomares-Millan H, Chen Y, Kurbasic A, Patel CJ, Renström F, Hallmans G, Johansson I, Franks PW. Exposome-wide ranking of modifiable risk factors for cardiometabolic disease traits. Sci Rep. 2022;12(1):4088.

    Article  ADS  CAS  PubMed  PubMed Central  Google Scholar 

  15. Marín D, Orozco LY, Narváez DM, Ortiz-Trujillo IC, Molina FJ, Ramos CD, Rodriguez-Villamizar L, Bangdiwala SI, Morales O, Cuellar M, Hernández LJ, Henao EA, Lopera V, Corredor A, Toro MV, Groot H, Villamil-Osorio M, Muñoz DA, Hincapié RC, Amaya F, Oviedo AI, López L, Morales-Betancourt R, Marín-Ochoa BE, Sánchez-García OE, Marín JS, Abad JM, Toro JC, Pinzón E, Builes JJ, Rueda ZV. Characterization of the external exposome and its contribution to the clinical respiratory and early biological effects in children: the PROMESA cohort study protocol. PLoS ONE. 2023;18(1):e0278836.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  16. Peeters S, Wang C, Bijnens EM, Bullens DMA, Fokkens WJ, Bachert C, Hellings PW, Nawrot TS, Seys SF. Association between outdoor air pollution and chronic rhinosinusitis patient reported outcomes. Environ Health. 2022;21(1):134.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  17. de Hoog MLA, Sluiter-Post JGC, Westerhof I, Fourie E, Heuvelman VD, Boom TT, Euser SM, Badoux P, Reusken C, Bont LJ, Sanders EAM, Jaddoe VWV, Herpers BL, Eggink D, Wildenbeest JG, Duijts L, van Houten MA, Bruijning-Verhagen PCJL. Longitudinal Household Assessment of respiratory illness in children and parents during the COVID-19 pandemic. JAMA Netw Open. 2022;5(10):e2237522.

    Article  PubMed  PubMed Central  Google Scholar 

  18. Juarez PD, Hood DB, Rogers GL, Baktash SH, Saxton AM, Matthews-Juarez P, Im W, Cifuentes MP, Phillips CA, Lichtveld MY, Langston MA. A novel approach to analyzing lung cancer mortality disparities: using the exposome and a graph-theoretical toolchain. Environ Dis. 2017 Apr-Jun;2(2):33–44.

  19. Gracia-Cazaña T, González S, Parrado C, Juarranz Á, Gilaberte Y. Influence of the exposome on skin cancer. La influencia del exposoma en El cáncer de piel. Actas Dermo-Sifiliogr. 2020;111(6):460–70.

    Article  Google Scholar 

  20. Monroy-Iglesias MJ, Dolly S, Sarker D, Thillai K, Van Hemelrijck M, Santaolalla A. Pancreatic cancer exposome profile to aid early detection and inform prevention strategies. J Clin Med. 2021;10(8):1665.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  21. Chen N, Liang H, Huang T, Huang N. Exposome approach for identifying modifiable factors for the prevention of colorectal cancer. Sci Rep. 2022;12(1):21615.

    Article  ADS  CAS  PubMed  PubMed Central  Google Scholar 

  22. Othman M, Latif MT, Matsumi Y. The exposure of children to PM2.5 and dust in indoor and outdoor school classrooms in Kuala Lumpur City Centre. Ecotoxicol Environ Saf. 2019;170:739–49.

    Article  CAS  PubMed  Google Scholar 

  23. Othman M, Latif MT, Yee CZ, Norshariffudin LK, Azhari A, Halim NDA, Alias A, Sofwan NM, Hamid HHA, Matsumi Y. PM2.5 and ozone in office environments and their potential impact on human health. Ecotoxicol Environ Saf. 2020;194:110432.

    Article  CAS  PubMed  Google Scholar 

  24. Sopian NA, Jalaludin J, Abu Bakar S, Hamedon TR, Latif MT. Exposure to particulate PAHs on potential genotoxicity and Cancer risk among School Children Living Near the Petrochemical Industry. Int J Environ Res Public Health. 2021;18(5):2575.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  25. Praveena SM. Characterization and Risk Analysis of Metals Associated with Urban Dust in Rawang (Malaysia). Arch Environ Contam Toxicol. 2018;75(3):415–23.

    Article  CAS  PubMed  Google Scholar 

  26. Yang J, Ching YC, Kadokami K, Ching KY, Xu S, Hu G, Wang J. Distribution and health risks of organic micropollutants from home dusts in Malaysia. Chemosphere. 2022;309(Pt 1):136600.

    Article  ADS  CAS  PubMed  Google Scholar 

  27. Zulkafflee NS, Mohd Redzuan NA, Nematbakhsh S, Selamat J, Ismail MR, Praveena SM, Yee Lee S, Abdull Razis AF. Heavy Metal Contamination in Oryza sativa L. at the Eastern Region of Malaysia and its risk Assessment. Int J Environ Res Public Health. 2022;19(2):739.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  28. Zulkafflee NS, Redzuan NAM, Selamat J, Ismail MR, Praveena SM, Razis AFA. Evaluation of Heavy Metal Contamination in Paddy Plants at the Northern Region of Malaysia using ICPMS and its risk Assessment. Plants (Basel). 2020;10(1):3.

    Article  CAS  PubMed  Google Scholar 

  29. Abdul Wahab S, Hassan A, Latif MT, Vadiveel Y, Jeyabalan T, Soo CI, Abdul Hamid F, Yu-Lin AB, Hassan T. Cluster analysis evaluating PM2.5, Occupation Risk and Mode of Transportation as surrogates for Air-pollution and the impact on Lung Cancer diagnosis and 1-Year mortality. Asian Pac J Cancer Prev. 2019;20(7):1959–65.

    Article  PubMed  PubMed Central  Google Scholar 

  30. Tricker AR, Preussmann R. Carcinogenic N-nitrosamines in the diet: occurrence, formation, mechanisms and carcinogenic potential. Mutat Res. 1991;259:277–89.

    Article  CAS  PubMed  Google Scholar 

  31. Li Y, Hecht SS. Metabolic activation and DNA interactions of carcinogenic N-Nitrosamines to which humans are commonly exposed. Int J Mol Sci. 2022;23:4559.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  32. Barbosa F Jr, Rocha BA, Souza MCO, Bocato MZ, Azevedo LF, Adeyemi JA, Santana A, Campiglia AD. Polycyclic aromatic hydrocarbons (PAHs): updated aspects of their determination, kinetics in the human body, and toxicity. J Toxicol Environ Health B Crit Rev. 2023;26(1):28–65.

    Article  CAS  PubMed  Google Scholar 

  33. Ranchoux B, Meloche J, Paulin R, Boucherat O, Provencher S, Bonnet S. DNA damage and pulmonary hypertension. Int J Mol Sci. 2016;17(6):990.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  34. Jia J, Bi C, Zhang J, Jin X, Chen Z. Characterization of polycyclic aromatic hydrocarbons (PAHs) in vegetables near industrial areas of Shanghai, China: sources, exposure, and cancer risk. Environ Pollut. 2018;241:750–8.

    Article  CAS  PubMed  Google Scholar 

  35. Zhu Y, Duan X, Qin N, Lv J, Wu G, Wei F. Health risk from dietary exposure to polycyclic aromatic hydrocarbons (PAHs) in a typical high cancer incidence area in southwest China. Sci Total Environ. 2019;649:731–8.

    Article  ADS  CAS  PubMed  Google Scholar 

  36. Jiang D, Wang G, Li L, Wang X, Li W, Li X, Shao L, Li F. Occurrence, dietary exposure, and health risk estimation of polycyclic aromatic hydrocarbons in grilled and fried meats in Shandong of China. Food Sci Nutr. 2018;6(8):2431–9.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  37. Kang HJ, Lee SY, Lee DY, Kang JH, Kim JH, Kim HW, Oh DH, Jeong JW, Hur SJ. Main mechanisms for carcinogenic heterocyclic amine reduction in cooked meat by natural materials. Meat Sci. 2022;183:108663.

    Article  CAS  PubMed  Google Scholar 

  38. Bellamri M, Walmsley SJ, Turesky RJ. Metabolism and biomarkers of heterocyclic aromatic amines in humans. Genes Environ. 2021;43(1):29.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  39. Wang P, Hong Y, Ke W, Hu X, Chen F. Formation of heterocyclic amines in Chinese marinated meat: effects of animal species and ingredients (rock candy, soy sauce and rice wine). J Sci Food Agric. 2017;97(12):3967–78.

    Article  CAS  PubMed  Google Scholar 

  40. Jahurul MHA, Jinap S, Ang SJ, Abdul-Hamid A, Hajeb P, Lioe HN, Zaidul ISM. Dietary exposure to heterocyclic amines in high-temperature cooked meat and fish in Malaysia. Food Addit Contam Part Chem Anal Control Expo Risk Assess. 2010;27(8):1060–71.

    Article  CAS  Google Scholar 

  41. Friedman MA, Dulak LH, Stedham MA. A lifetime oncogenicity study in rats with acrylamide. Toxicol Sci. 1995;27(1):95–105.

    Article  CAS  Google Scholar 

  42. Ji K, Kang S, Lee G, Lee S, Jo A, Kwak K, Kim D, Kho D, Lee S, Kim S, et al. Urinary levels of N-acetyl-S-(2-carbamoylethyl)-cysteine (AAMA), an acrylamide metabolite, in Korean children and their association with food consumption. Sci Total Environ. 2013;456–457:17–23.

    Article  ADS  PubMed  Google Scholar 

  43. Kotemori A, Ishihara J, Zha L, Liu R, Sawada N, Iwasaki M, Sobue T, Tsugane S, JPHC Study Group. Dietary acrylamide intake and risk of breast cancer: the Japan Public Health Center-based prospective study. Cancer Sci. 2018;109(3):843–53.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  44. Liu R, Sobue T, Kitamura T, Kitamura Y, Ishihara J, Kotemori A, Zha L, Ikeda S, Sawada N, Iwasaki M, Tsugane S, of the JPHC Study Group. Dietary acrylamide intake and risk of esophageal, gastric, and Colorectal Cancer: the Japan Public Health Center-based prospective study. Cancer Epidemiol Biomarkers Prev. 2019;28(9):1461–8.

    Article  PubMed  Google Scholar 

  45. Liu R, Zha L, Sobue T, Kitamura T, Ishihara J, Kotemori A, Ikeda S, Sawada N, Iwasaki M, Tsugane S. Dietary acrylamide intake and risk of Lung Cancer: the Japan Public Health Center Based Prospective Study. Nutrients. 2020;12(8):2417.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  46. Zha L, Sobue T, Kitamura T, Kitamura Y, Ishihara J, Kotemori A, Liu R, Ikeda S, Sawada N, Iwasaki M, Tsugane S, Jphc Study Group FT. Dietary acrylamide intake and the risk of Liver Cancer: the Japan Public Health Center-based prospective study. Nutrients. 2020;12(9):2503.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  47. Kito K, Ishihara J, Kotemori A, Zha L, Liu R, Sawada N, Iwasaki M, Sobue T, Tsugane S. Dietary acrylamide intake and the risk of pancreatic Cancer: the Japan Public Health Center-based prospective study. Nutrients. 2020;12(11):3584.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  48. Hogervorst JG, Schouten LJ, Konings EJ, Goldbohm RA, van den Brandt PA. A prospective study of dietary acrylamide intake and the risk of endometrial, ovarian, and breast cancer. Cancer Epidemiol Biomarkers Prev. 2007;16(11):2304–13.

    Article  CAS  PubMed  Google Scholar 

  49. Lipunova N, Schouten LJ, van den Brandt PA, Hogervorst JG. A prospective cohort study on dietary acrylamide intake and the risk for cutaneous malignant melanoma. Eur J Cancer Prev. 2016;26(6):528–31.

    Article  Google Scholar 

  50. Bongers ML, Hogervorst JG, Schouten LJ, Goldbohm RA, Schouten HC, van den Brandt PA. Dietary acrylamide intake and the risk of lymphatic malignancies: the Netherlands Cohort Study on diet and cancer. PLoS ONE. 2012;7(6):e38016.

    Article  ADS  CAS  PubMed  PubMed Central  Google Scholar 

  51. Iwasaki M, Itoh H, Sawada N, Tsugane S. Exposure to environmental chemicals and cancer risk: epidemiological evidence from Japanese studies. Genes Environ. 2023;45(1):10.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  52. Nur Fatihah MN, Sharif R. 2018. Health Risk Assessment of Acrylamide in Deep Fried Starchy Foods among Students of Kolej Tun Syed Nasir, Universiti Kebangsaan Malaysia. Jurnal Sains Kesihatan Malaysia 16(2) 2018: 113–117.

  53. Shafiee NH, Razalli NH, Shahril MR, Muhammad Nawawi KN, Mohd Mokhtar N, Abd Rashid AA, Ashari LS, Jan Mohamed HJ, Raja Ali RA. Dietary inflammatory index, obesity, and the incidence of Colorectal Cancer: findings from a hospital-based case-control study in Malaysia. Nutrients. 2023;15(4):982.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  54. Abd Rashid AA, Ashari LS, Shafiee NH, Raja Ali RA, Yeong Yeh L, Shahril MR, Jan Mohamed HJ. Dietary patterns associated with colorectal cancer risk in the Malaysian population: a case-control study with exploratory factor and regression analysis. BMC Public Health. 2023;23(1):1386.

    Article  PubMed  PubMed Central  Google Scholar 

  55. Sharif R, Mohammad NMA, Jia Xin Y, Abdul Hamid NH, Shahar S, Ali RAR. Dietary risk factors and odds of colorectal adenoma in Malaysia: a Case Control Study. Nutr Cancer. 2022;74(8):2757–68.

    Article  CAS  PubMed  Google Scholar 

  56. Barrett D, Ploner A, Chang ET, Liu Z, Zhang CX, Liu Q, Cai Y, Zhang Z, Chen G, Huang QH, Xie SH, Cao SM, Shao JY, Jia WH, Zheng Y, Liao J, Chen Y, Lin L, Ernberg I, Adami HO, Huang G, Zeng Y, Zeng YX, Ye W. Past and recent salted fish and Preserved Food Intakes Are Weakly Associated with nasopharyngeal carcinoma risk in adults in Southern China. J Nutr. 2019;149(9):1596–605.

    Article  PubMed  PubMed Central  Google Scholar 

  57. Armstrong RW, Eng AC. Salted fish and nasopharyngeal carcinoma in Malaysia. Soc Sci Med. 1983;17(20):1559–67.

    Article  CAS  PubMed  Google Scholar 

  58. Armstrong RW, Armstrong MJ, Yu MC, Henderson BE. Salted fish and inhalants as risk factors for nasopharyngeal carcinoma in Malaysian Chinese. Cancer Res. 1983;43(6):2967–70.

    CAS  PubMed  Google Scholar 

  59. Yu MC, Ho JH, Henderson BE, Armstrong RW. Epidemiology of nasopharyngeal carcinoma in Malaysia and Hong Kong. Natl Cancer Inst Monogr. 1985;69:203–7.

    CAS  PubMed  Google Scholar 

  60. Sharif R, Ghazali AR, Rajab NF, Haron H, Osman F. Toxicological evaluation of some Malaysian locally processed raw food products. Food Chem Toxicol. 2008;46(1):368–74.

    Article  CAS  PubMed  Google Scholar 

  61. Mohammad N, Yusoff N, Zulfakar S, Sharif R. Evaluation of mutagenic profile of shrimp paste extracts by using Ames test. Pakistan J Nutr. 2016;15(2):170–5.

    Article  CAS  Google Scholar 

  62. Sanusi MSM, Ramli AT, Hashim S, Lee MH. Radiological hazard associated with amang processing industry in Peninsular Malaysia and its environmental impacts. Ecotoxicol Environ Saf. 2021;208:111727.

    Article  CAS  PubMed  Google Scholar 

  63. Eshkoor SA, Marashi SJ, Ismail P, Rahman SA, Mirinargesi M, Adon MY, Devan RV. Association of GSTM1 and GSTT1 with ageing in auto repair shop workers. Genet Mol Res. 2012;11(2):1486–96.

    Article  CAS  PubMed  Google Scholar 

  64. How V, Hashim Z, Ismail P, Omar D, Said SM, Tamrin SB. Characterization of risk factors for DNA damage among paddy farm worker exposed to mixtures of organophosphates. Arch Environ Occup Health. 2015;70(2):102–9.

    Article  CAS  PubMed  Google Scholar 

  65. Ahmad MH, Man CS, Othman F, He FJ, Salleh R, Noor NSM, Kozil WNKW, MacGregor G, Aris T. High sodium food consumption pattern among Malaysian population. J Health Popul Nutr. 2021;40(Suppl 1):4.

    Article  PubMed  PubMed Central  Google Scholar 

  66. Bruni L, Diaz M, Castellsagué M, et al. Cervical human papillomavirus prevalence in 5 continents: Meta-Analysis of 1 million women with normal cytological findings. J Infect Dis. 2010;202:1789–99.

    Article  PubMed  Google Scholar 

  67. Williamson AL. Recent developments in human papillomavirus (HPV) vaccinology. Viruses. 2023;15(7):1440.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  68. Rahmat F, Kuan JY, Hajiman Z, Mohamed Shakrin NNS, Che Roos NA, Mustapa M, Ahmad Zaidi NA, Ahmad A. Human papillomavirus (HPV) prevalence and type distribution in Urban areas of Malaysia. Asian Pac J Cancer Prev. 2021;22(9):2969–76.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  69. Sainei NE, Kumar VS, Chin YS, Salih FAM. High prevalence of human papillomavirus types 56 and 70 identified in the native populations of Sabah, Malaysia. Asian Pac J Cancer Prev. 2018;19(10):2807–13.

    CAS  PubMed  PubMed Central  Google Scholar 

  70. Hastert TA, Beresford SA, Sheppard L, White E. Disparities in cancer incidence and mortality by area-level socioeconomic status: a multilevel analysis. J Epidemiol Community Health. 2015;69(2):168–76.

    Article  PubMed  Google Scholar 

  71. Carethers JM, Doubeni CA. Causes of socioeconomic disparities in colorectal Cancer and intervention Framework and Strategies. Gastroenterology. 2020;158(2):354–67.

    Article  PubMed  Google Scholar 

Download references


Not applicable.


Ministry of Higher Education grant (FRGS/1/2020/STG02/UKM/02/5).

Author information

Authors and Affiliations



RS drafted, searched and written the whole article.

Corresponding author

Correspondence to Razinah Sharif.

Ethics declarations

Competing interests

The authors declare that they have no competing interests.

Additional information

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Sharif, R., Ooi, T.C. Understanding exposomes and its relation with cancer risk in Malaysia based on epidemiological evidence: a narrative review. Genes and Environ 46, 5 (2024).

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: