Displaying publications 61 - 80 of 110 in total

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  1. Md Sani ND, Ariffin EY, Sheryn W, Shamsuddin MA, Heng LY, Latip J, et al.
    Sensors (Basel), 2019 Nov 22;19(23).
    PMID: 31766637 DOI: 10.3390/s19235111
    A toxicity electrochemical DNA biosensor has been constructed for the detection of carcinogens using 24 base guanine DNA rich single stranded DNA, and methylene blue (MB) as the electroactive indicator. This amine terminated ssDNA was immobilized onto silica nanospheres and deposited on gold nanoparticle modified carbon-paste screen printed electrodes (SPEs). The modified SPE was initially exposed to a carcinogen, followed by immersion in methylene blue for an optimized duration. The biosensor response was measured using differential pulse voltammetry. The performance of the biosensor was identified on several anti-cancer compounds. The toxicity DNA biosensor demonstrated a linear response range to the cadmium chloride from 0.0005 ppm to 0.01 ppm (R2 = 0.928) with a limit of detection at 0.0004 ppm. The biosensor also exhibited its versatility to screen the carcinogenicity of potential anti-cancer compounds.
    Matched MeSH terms: Carcinogens/chemistry*
  2. Mohd Mahathir Suhaimi Shamsuri, Leman, A.M.
    MyJurnal
    Indoor pollution increasingly becomes a public concern. These concerns are related to energy efficiency in a
    building. There are various ways in which it can ensure energy conservation can be achieved, including superinsulation
    and reduced fresh air exchange. As a result, indoor air becomes stagnant and odours, thereafter contaminants of air will
    accumulate and will certainly disrupt human health. It is quite difficult to make people comfortable in a building with
    consumption of energy-saving and human health guaranteed. Indoor plants are one of the alternative solutions that
    have been studied since the last three decades. This paper intends to review the abilities of indoor plants to purify air,
    and the ways used by previous researchers to prove that indoor plants can treat the air. In general, it can be stated that
    indoor plants are able to absorb various types of volatile organic compounds (VOCs). An advantage of indoor plants
    to cure air from carcinogen gas is greatly needed for human health. Therefore, studies on indoor plants to neutralize
    the air are gaining attention. Enclosed space or chamber is often used by researchers to test the ability of indoor plants
    absorb gaseous toxins in their study; because it is easy to handle and can quickly determine the absorption rate. In the
    other hand, environmental factors such as temperature, humidity, and light are important to be taken into consideration
    during the study. As a conclusion, it can be stated that the existence of indoor plants in a building is very reasonable,
    because it can give positive impacts on human health and the total energy consumption.
    Matched MeSH terms: Carcinogens
  3. Mohd Shahrol Abd Wahil, Wong, Chin Mun, Abdullah Aliff Abdul Wahab, Hasni Ja’afar
    MyJurnal
    Malaysia is the world’s third largest exporter of liquified natural gas and the second largest oil and natural gas producer in Southeast Asia, following Indonesia. The potential air pollutants released from the industry may affect the health of the population. The primary objective of this study was to determine the potential health risk among the population in the zone of impact. This was a comparative case study between controlled and uncontrolled emissions based on the air dispersion modelling. Hazard quotient (HQ) was used to assess non-carcinogenic risk, while lifetime cancer risk (LCR) was used to assess carcinogenic risk. All ambient air pollutant levels were within permissible levels and adhered to the standard. The HQ for hydrogen sulphide and benzene was less than one in all scenarios. The LCR for benzene was acceptable in all scenarios. Advanced pollution prevention equipment should be installed within the gas emission system to treat the final emission to meet prescribed permissible limits. Continuous ambient air monitoring and effective control measures should be practiced to ensure the sustainability of clean air. The health risk assessment showed no risk of developing malignancy and non-cancer disorder among the workers and general population living surround the petrochemical plants. This allows the development of the petroleum refinery plants to be continued.
    Matched MeSH terms: Carcinogens
  4. Motorykin O, Matzke MM, Waters KM, Massey Simonich SL
    Environ Sci Technol, 2013 Apr 2;47(7):3410-6.
    PMID: 23472838 DOI: 10.1021/es305295d
    The objective of this research was to investigate the relationship between lung cancer mortality rates, carcinogenic polycyclic aromatic hydrocarbon (PAH) emissions, and smoking on a global scale, as well as for different socioeconomic country groups. The estimated lung cancer deaths per 100,000 people (ED100000) and age standardized lung cancer death rate per 100,000 people (ASDR100000) in 2004 were regressed on PAH emissions in benzo[a]pyrene equivalence (BaPeq), smoking prevalence, cigarette price, gross domestic product per capita, percentage of people with diabetes, and average body mass index using simple and multiple linear regression for 136 countries. Using stepwise multiple linear regression, a statistically significant positive linear relationship was found between loge(ED100000) and loge(BaPeq) emissions for high (p-value <0.01) and for the combination of upper-middle and high (p-value <0.05) socioeconomic country groups. A similar relationship was found between loge(ASDR100000) and loge(BaPeq) emissions for the combination of upper-middle and high (p-value <0.01) socioeconomic country groups. Conversely, for loge(ED100000) and loge(ASDR100000), smoking prevalence was the only significant independent variable in the low socioeconomic country group (p-value <0.001). These results suggest that reducing BaPeq emissions in the U.S., Canada, Australia, France, Germany, Brazil, South Africa, Poland, Mexico, and Malaysia could reduce ED100000, while reducing smoking prevalence in Democratic People's Republic of Korea, Nepal, Mongolia, Cambodia, and Bangladesh could significantly reduce the ED100000 and ASDR100000.
    Matched MeSH terms: Carcinogens/analysis*
  5. Muhammad Adil Zainal Abidin, Hayati Kadir Shahar, Rosliza Abdul Manaf
    MyJurnal
    Introduction: Secondhand tobacco smoke is a known carcinogen and has shown positive association with smok-ing status, susceptibility and cessation. Smoke free environment policy seem to reduce this exposure and influence intention to quit and frequency of quit attempts. Despite having a smoke free policy, smokers are still exposed to second hand smoke and this might influence their smoking behaviour and cessation. The objective of this study was to examine the association between environmental tobacco smoke exposures with intention to quit smoking among young adults in college with smoke free policy. Methods: Data were drawn from a cluster based randomised controlled trial in 10 government colleges in Selangor. Baseline characteristics of 160 college smokers were mea-sured using adapted questionnaire. Intention to quit was measured using Transtheoretical Model and environmental influence of tobacco smoke exposure. Results: Majority of the smokers were male (99.4%), single (100%), of Malay ethnicity (94.4%) and Muslim (95.6%). Most of them are in pre-contemplation stage where they do not have any intention to quit (65.6%). On environmental influence, at work or college environmental exposure, majority were exposed between 1 to 2 hours (36.9%) and 3 to 8 hours (40.6%). On exposure at home or hostel, majority were exposed between 1 to 4 hours (44.4%) and 5 to 14 hours (21.9%). In terms of friend’s exposures, majority have most of their friends smoking (68.1%). We found no statistically significant association between environmental influence and intention to quit smoking. Conclusion: Although we found no relationship, future research should examine the pathway between environmental influence and smoking behaviour.
    Matched MeSH terms: Carcinogens
  6. Narayanan KB, Ali M, Barclay BJ, Cheng QS, D'Abronzo L, Dornetshuber-Fleiss R, et al.
    Carcinogenesis, 2015 Jun;36 Suppl 1:S89-110.
    PMID: 26106145 DOI: 10.1093/carcin/bgv032
    Cell death is a process of dying within biological cells that are ceasing to function. This process is essential in regulating organism development, tissue homeostasis, and to eliminate cells in the body that are irreparably damaged. In general, dysfunction in normal cellular death is tightly linked to cancer progression. Specifically, the up-regulation of pro-survival factors, including oncogenic factors and antiapoptotic signaling pathways, and the down-regulation of pro-apoptotic factors, including tumor suppressive factors, confers resistance to cell death in tumor cells, which supports the emergence of a fully immortalized cellular phenotype. This review considers the potential relevance of ubiquitous environmental chemical exposures that have been shown to disrupt key pathways and mechanisms associated with this sort of dysfunction. Specifically, bisphenol A, chlorothalonil, dibutyl phthalate, dichlorvos, lindane, linuron, methoxychlor and oxyfluorfen are discussed as prototypical chemical disruptors; as their effects relate to resistance to cell death, as constituents within environmental mixtures and as potential contributors to environmental carcinogenesis.
    Matched MeSH terms: Carcinogens, Environmental/adverse effects*
  7. Nor WMFSBW, Chung I, Said NABM
    Oncol Res, 2020 Oct 27.
    PMID: 33109304 DOI: 10.3727/096504020X16037933185170
    Breast cancer is the most commonly diagnosed cancer among women and one of the leading causes of cancer mortality worldwide, in which the most severe form happens when it metastasizes to other regions of the body. Metastasis is responsible for most treatment failures in advanced breast cancer. Epithelial-mesenchymal transition (EMT) plays a significant role in promoting metastatic processes in breast cancer. MicroRNAs (miRNAs) are highly conserved endogenous short non-coding RNAs that play a role in regulating a broad range of biological processes, including cancer initiation and development, by functioning as tumor promoters or tumor suppressors. Expression of miR-548m has been found in various types of cancers, but the biological function and molecular mechanisms of miR-548m in cancers have not been fully studied. Here, we demonstrated the role of miR-548m in modulating EMT in the breast cancer cell lines MDA-MB-231 and MCF-7. Expression data for primary breast cancer obtained from NCBI GEO datasets showed that miR-548m expression was downregulated in breast cancer patients compared with healthy group. We hypothesize that miR-548m acts as a tumor suppressor in breast cancer. Overexpression of miR-548m in both cell lines increased E-cadherin expression and decreased the EMT-associated transcription factors SNAI1, SNAI2, ZEB1 and ZEB2, as well as MMP9 expression. Consequently, migration and invasion capabilities of both MDA-MB-231 and MCF-7 cells were significantly inhibited in miR-548m-overexpressing cells. Analysis of 1059 putative target genes of miR-548m revealed common pathways involving both tight junction and the mTOR signaling pathway, which has potential impacts on cell migration and invasion. Furthermore, this study identified aryl hydrocarbon receptor (AHR) as a direct target of miR-548m in breast cancer cells. Taken together, our findings suggest a novel function of miR-548m in reversing the EMT of breast cancer by reducing their migratory and invasive potentials, at least in part via targeting AHR expression.
    Matched MeSH terms: Carcinogens
  8. Norazalina S, Norhaizan ME, Hairuszah I, Norashareena MS
    Exp. Toxicol. Pathol., 2010 May;62(3):259-68.
    PMID: 19464858 DOI: 10.1016/j.etp.2009.04.002
    This study is carried out to determine the potential of phytic acid extracted from rice bran in the suppression of colon carcinogenesis induced by azoxymethane (AOM) in rats. Seventy-two male Sprague-Dawley rats were divided into 6 groups with 12 rats in each group. The intended rats for cancer treatment received two intraperitoneal injections of AOM in saline (15mg/kg bodyweight) over a 2-week period. The treatments of phytic acid were given in two concentrations: 0.2% (w/v) and 0.5% (w/v) during the post-initiation phase of carcinogenesis phase via drinking water. The colons of the animals were analyzed for detection and quantification of aberrant crypt foci (ACF) after 8 weeks of treatment. The finding showed treatment with 0.2% (w/v) extract phytic acid (EPA) gave the greatest reduction in the formation of ACF. In addition, phytic acid significantly suppressed the number of ACF in the distal, middle and proximal colon as compared to AOM alone (p<0.05). For the histological classification of ACF, treatment with 0.5% (w/v) commercial phytic acid (CPA) had the highest percentage (71%) of non-dysplastic ACF followed by treatment with 0.2% (w/v) EPA (61%). Administration of phytic acid also reduced the incidence and multiplicity of total tumors even though there were no significant differences between groups. In conclusion, this study found the potential value of phytic acid extracted from rice bran in reducing colon cancer risk in rats.
    Matched MeSH terms: Carcinogens/toxicity
  9. Norhanom AW, Yadav M
    Br. J. Cancer, 1995 Apr;71(4):776-9.
    PMID: 7710943
    Herbal medication has been practised by the rural Malaysian Malays for a long time. However, the long-term side-effects have never been studied. In the present study, 48 species of Euphorbiaceae were screened for tumour-promoter activity by means of an in vitro assay using a human lymphoblastoid cell line harbouring the Epstein-Barr virus (EBV) genome. Twenty-seven per cent (13 out of 48) of the species tested were found to be positive, and in four species, namely Breynia coronata Hk.f, Codiaeum variegatum (L) Bl, Euphorbia atoto and Exocoecaria agallocha, EBV-inducing activity was observed when the plant extracts were tested at low concentrations of between 0.2 and 1.2 micrograms ml-1 in cell culture. This observation warrants attention from the regular users of these plants because regular use of plants with tumour-promoting activity could well be an aetiological factor for the promotion of tumours among rural Malaysian Malays.
    Matched MeSH terms: Carcinogens*
  10. Nur Hidayah J, Abdul Razis AF, Jambari NN, Chai LC, You L, Sanny M
    Food Chem Toxicol, 2024 Mar;185:114502.
    PMID: 38346572 DOI: 10.1016/j.fct.2024.114502
    This study aimed to estimate the Malaysian adult population's current dietary exposure and margin of exposure (MOE) to the carcinogenic processing contaminant, acrylamide. A total of 448 samples from 11 types of processed foods were collected randomly throughout Malaysia in the year 2015 and 2016. Acrylamide was analysed in samples using Liquid Chromatography-Tandem Mass Spectrometry (LC-MS/MS) with a limit of detection (LOD) of 10 μg/kg and a limit of quantification (LOQ) of 25 μg/kg. The highest average level of acrylamide (772 ± 752 μg/kg) was found in potato crisps, followed by French fries (415 ± 914 μg/kg) and biscuits (245 ± 195 μg/kg). The total acrylamide exposure for the adult Malaysian was 0.229 and 1.77 μg/kg body weight per day for average and high consumers, respectively. The MOE were 741 and 1875 for the average consumer based on cancer and non-cancer effects of acrylamide, respectively. Meanwhile, for high consumers, the MOE is 96 for cancer and 243 for non-cancer effects. These findings indicate potential carcinogenic risks from acrylamide exposure among Malaysian adults, especially in Malay and other Bumiputra groups compared to Chinese, Indian, and other ethnic groups, while non-cancer effects appeared less concerning.
    Matched MeSH terms: Carcinogens/analysis; Carcinogens/toxicity
  11. Ochieng J, Nangami GN, Ogunkua O, Miousse IR, Koturbash I, Odero-Marah V, et al.
    Carcinogenesis, 2015 Jun;36 Suppl 1:S128-59.
    PMID: 26106135 DOI: 10.1093/carcin/bgv034
    The purpose of this review is to stimulate new ideas regarding low-dose environmental mixtures and carcinogens and their potential to promote invasion and metastasis. Whereas a number of chapters in this review are devoted to the role of low-dose environmental mixtures and carcinogens in the promotion of invasion and metastasis in specific tumors such as breast and prostate, the overarching theme is the role of low-dose carcinogens in the progression of cancer stem cells. It is becoming clearer that cancer stem cells in a tumor are the ones that assume invasive properties and colonize distant organs. Therefore, low-dose contaminants that trigger epithelial-mesenchymal transition, for example, in these cells are of particular interest in this review. This we hope will lead to the collaboration between scientists who have dedicated their professional life to the study of carcinogens and those whose interests are exclusively in the arena of tissue invasion and metastasis.
    Matched MeSH terms: Carcinogens, Environmental/adverse effects*
  12. Ong FB, Wan Ngah WZ, Top AG, Khalid BA, Shamaan NA
    Int. J. Biochem., 1994 Mar;26(3):397-402.
    PMID: 7910569
    1. The effects of alpha-tocopherol and gamma-tocotrienol on glutathione S-transferase (GST) and gamma-glutamyl transpeptidase (gamma-GT) activities in cultured hepatocytes prepared from rats treated with diethylnitrosamine (DEN) and 2-acetylaminofluorene (AAF) were investigated. 2. Both the alpha-tocopherol and gamma-tocotrienol treated hepatocytes showed significantly higher (P < 0.05) GST activities than untreated hepatocytes prepared from the carcinogen treated rats in the first 3 days of culture. Treatment with alpha-tocopherol and gamma-tocotrienol generally resulted in a tendency to increase the GST activities above that in the untreated hepatocytes. 3. Treatment with high doses (125-250 microM) of alpha-tocopherol and low doses (12.5-25 microM) of gamma-tocotrienol generally resulted in a significant reduction in gamma-GT activities at 1-3 days. gamma-GT activities are reduced as the dose of alpha-tocopherol and gamma-tocotrienol are increased.
    Matched MeSH terms: Carcinogens/toxicity*
  13. Panda BP, Mohanta YK, Parida SP, Pradhan A, Mohanta TK, Patowary K, et al.
    Environ Pollut, 2023 Aug 01;330:121796.
    PMID: 37169242 DOI: 10.1016/j.envpol.2023.121796
    Metals are micropollutants that cannot be degraded by microorganisms and are infiltrated into various environmental media, including both freshwater and marine water. Metals from polluted water are absorbed by many aquatic species, especially fish. Fish is a staple food in the diets of many regions in the world; hence, both the type and concentration of metals accumulated and transferred from contaminated water sources to fish must be determined and assessed. In this study, the heavy metal concentration was determined and assessed in fish collected from freshwater sources via published literature and Estimated Daily Intake (EDI), Target hazard quotient (THQ), and Carcinogenic Risk (CR) analyses, aiming to examine the metal pollution in freshwater fish. The fish was used as a bioindicator, and Geographic information system (GIS) was sued to map the polluted regions. The results confirmed that Pb was detected in fish sampled at 28 locations, Cr at 24 locations, Cu and Zn at 30 locations, with values Pb detected ranging from 0.0016 mg kg-1 to 44.3 mg kg-1, Cr detected ranging from 0.07 mg kg-1 to 27 mg kg-1, Cu detected ranging from 0.031 mg kg-1 to 35.54 mg kg-1, and Zn detected ranging from 0.242 mg kg-1 to 103.2 mg kg-1. The strongest positive associations were discovered between Cu-Zn (r = 0.74, p 
    Matched MeSH terms: Carcinogens/analysis
  14. Pedersen M, Stafoggia M, Weinmayr G, Andersen ZJ, Galassi C, Sommar J, et al.
    Eur Urol Focus, 2018 01;4(1):113-120.
    PMID: 28753823 DOI: 10.1016/j.euf.2016.11.008
    BACKGROUND: Ambient air pollution contains low concentrations of carcinogens implicated in the etiology of urinary bladder cancer (BC). Little is known about whether exposure to air pollution influences BC in the general population.

    OBJECTIVE: To evaluate the association between long-term exposure to ambient air pollution and BC incidence.

    DESIGN, SETTING, AND PARTICIPANTS: We obtained data from 15 population-based cohorts enrolled between 1985 and 2005 in eight European countries (N=303431; mean follow-up 14.1 yr). We estimated exposure to nitrogen oxides (NO2 and NOx), particulate matter (PM) with diameter <10μm (PM10), <2.5μm (PM2.5), between 2.5 and 10μm (PM2.5-10), PM2.5absorbance (soot), elemental constituents of PM, organic carbon, and traffic density at baseline home addresses using standardized land-use regression models from the European Study of Cohorts for Air Pollution Effects project.

    OUTCOME MEASUREMENTS AND STATISTICAL ANALYSIS: We used Cox proportional-hazards models with adjustment for potential confounders for cohort-specific analyses and meta-analyses to estimate summary hazard ratios (HRs) for BC incidence.

    RESULTS AND LIMITATIONS: During follow-up, 943 incident BC cases were diagnosed. In the meta-analysis, none of the exposures were associated with BC risk. The summary HRs associated with a 10-μg/m3 increase in NO2 and 5-μg/m3 increase in PM2.5 were 0.98 (95% confidence interval [CI] 0.89-1.08) and 0.86 (95% CI 0.63-1.18), respectively. Limitations include the lack of information about lifetime exposure.

    CONCLUSIONS: There was no evidence of an association between exposure to outdoor air pollution levels at place of residence and risk of BC.

    PATIENT SUMMARY: We assessed the link between outdoor air pollution at place of residence and bladder cancer using the largest study population to date and extensive assessment of exposure and comprehensive data on personal risk factors such as smoking. We found no association between the levels of outdoor air pollution at place of residence and bladder cancer risk.

    Matched MeSH terms: Carcinogens, Environmental/adverse effects*
  15. Perkins AN, Inayat-Hussain SH, Deziel NC, Johnson CH, Ferguson SS, Garcia-Milian R, et al.
    Environ Res, 2019 02;169:163-172.
    PMID: 30458352 DOI: 10.1016/j.envres.2018.10.018
    Currently, there are >11,000 synthetic turf athletic fields in the United States and >13,000 in Europe. Concerns have been raised about exposure to carcinogenic chemicals resulting from contact with synthetic turf fields, particularly the infill material ("crumb rubber"), which is commonly fabricated from recycled tires. However, exposure data are scant, and the limited existing exposure studies have focused on a small subset of crumb rubber components. Our objective was to evaluate the carcinogenic potential of a broad range of chemical components of crumb rubber infill using computational toxicology and regulatory agency classifications from the United States Environmental Protection Agency (US EPA) and European Chemicals Agency (ECHA) to inform future exposure studies and risk analyses. Through a literature review, we identified 306 chemical constituents of crumb rubber infill from 20 publications. Utilizing ADMET Predictor™, a computational program to predict carcinogenicity and genotoxicity, 197 of the identified 306 chemicals met our a priori carcinogenicity criteria. Of these, 52 chemicals were also classified as known, presumed or suspected carcinogens by the US EPA and ECHA. Of the remaining 109 chemicals which were not predicted to be carcinogenic by our computational toxicology analysis, only 6 chemicals were classified as presumed or suspected human carcinogens by US EPA or ECHA. Importantly, the majority of crumb rubber constituents were not listed in the US EPA (n = 207) and ECHA (n = 262) databases, likely due to an absence of evaluation or insufficient information for a reliable carcinogenicity classification. By employing a cancer hazard scoring system to the chemicals which were predicted and classified by the computational analysis and government databases, several high priority carcinogens were identified, including benzene, benzidine, benzo(a)pyrene, trichloroethylene and vinyl chloride. Our findings demonstrate that computational toxicology assessment in conjunction with government classifications can be used to prioritize hazardous chemicals for future exposure monitoring studies for users of synthetic turf fields. This approach could be extended to other compounds or toxicity endpoints.
    Matched MeSH terms: Carcinogens*
  16. Praveena SM
    Arch Environ Contam Toxicol, 2018 Oct;75(3):415-423.
    PMID: 29802419 DOI: 10.1007/s00244-018-0537-7
    This study was designed to determine the particle size distribution and develop road dust index combining source and transport factors involving road dust for dust pollution quantification in Rawang. Principal component analysis (PCA) was applied to identify possible sources of potentially toxic elements and spot major pollution areas in Rawang. The health risks (carcinogenic and noncarcinogenic) to adults and children were assessed using the hazard index and total lifetime cancer Risk, respectively. A total of 75 road dust samples were collected and particle sizes (1000, 500, 250, 160, 125 and 63 µm) were determined. Concentrations of potentially toxic elements (Cu, Cd, Co, Cr, Pb, Ni, Zn and As) in particle size of 63 µm were analyzed. The results demonstrated that the highest grain size of 250 µm has contributed almost more than 25% of atmospheric particulate pollution. The highest potentially toxic element concentration was Pb (593.3 mg/kg), whereas the lowest was Co (5.6 mg/kg). Road dust index output indicated that pollution risk fell into moderate levels in eastern and northern areas of Rawang. Similarly, PCA results revealed that potentially toxic elements (Cu, Cd, Pb, Zn, Ni and Cr) were linked with anthropogenic sources (urbanization process, industrial and commercial growth, urban traffic congestion) in northern and southern parts of Rawang. Cobalt and As concentrations were explained mainly from natural sources. Noncarcinogenic risk by hazard index 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.
    Matched MeSH terms: Carcinogens
  17. Praveena SM, Aris AZ
    Environ Geochem Health, 2018 Apr;40(2):749-762.
    PMID: 28929262 DOI: 10.1007/s10653-017-0021-8
    This study aims to determine the status of potentially toxic element concentrations of road dust in a medium-sized city (Rawang, Malaysia). This study adopts source identification via enrichment factor, Pearson correlation analysis, and Fourier spectral analysis to identify sources of potentially toxic element concentrations in road dust in Rawang City, Malaysia. Health risk assessment was conducted to determine potential health risks (carcinogenic and non-carcinogenic risks) among adults and children via multiple pathways (i.e., ingestion, dermal contact, and inhalation). Mean of potentially toxic element concentrations were found in the order of Pb > Zn > Cr(IV) > Cu > Ni > Cd > As > Co. Source identification revealed that Cu, Cd, Pb, Zn, Ni, and Cr(IV) are associated with anthropogenic sources in industrial and highly populated areas in northern and southern Rawang, cement factories in southern Rawang, as well as the rapid development and population growth in northwestern Rawang, which have resulted in high traffic congestion. Cobalt, Fe, and As are related to geological background and lithologies in Rawang. Pathway orders for both carcinogenic and non-carcinogenic risks are ingestion, dermal contact, and inhalation, involving adults and children. Non-carcinogenic health risks in adults were attributed to Cr(IV), Pb, and Cd, whereas Cu, Cd, Cr(IV), Pb, and Zn were found to have non-carcinogenic health risks for children. Cd, Cr(IV), Pb, and As may induce carcinogenic risks in adults and children, and the total lifetime cancer risk values exceeded incremental lifetime.
    Matched MeSH terms: Carcinogens/toxicity
  18. Raaschou-Nielsen O, Beelen R, Wang M, Hoek G, Andersen ZJ, Hoffmann B, et al.
    Environ Int, 2016 Feb;87:66-73.
    PMID: 26641521 DOI: 10.1016/j.envint.2015.11.007
    Particulate matter (PM) air pollution is a human lung carcinogen; however, the components responsible have not been identified. We assessed the associations between PM components and lung cancer incidence.
    Matched MeSH terms: Carcinogens
  19. Rahmat A, Wan Ngah WZ, Gapor A, Khalid BA
    Asia Pac J Clin Nutr, 1993 Sep;2(3):129-34.
    PMID: 24352144
    The effects of long-term administration of tocotrienol on hepatocarcinogenesis in rats induced by diethyl nitrosamine (DEN) and 2-acetylaminofluorene (AAF) were investigated by the determination of plasma and liver gamma-glutamyl transpeptidase (GGT), cytosolic glutathione reductase (GSSG-Rx), glutathione peroxidase (GSH-Px) and glutathione S-transferase (GST). Twenty-eight male Rattus norwegicus rats (120-160g) were divided according to treatments into four groups: control group, tocotrienol - supplemented diet group (30mg/kg food), DEN/AAF-treated group and DEN/AAF treated plus tocotrienol-supplemented-diet group (30mg/kg food). The rats were sacrificed after nine months. The results obtained indicated no difference in the morphology and histology of the livers of control and tocotrienol-treated rats. Greyish-white neoplastic nodules (two per liver) were found in all the DEN/ AAF treated rats (n-10) whereas only one nodule was found in one of the carcinogen treated rats receiving tocotrienol supplementation (n-6). Histological examination showed obvious cellular damage for both the DEN/AAF-treated rats and the tocotrienol-supplemented rats but were less severe in the latter. Treatment with DEN/AAF caused increases in GGT, GSH-Px, GST and GSSG-Rx activities when compared to controls. These increases were also observed when tocotrienol was supplemented with DEN/AAF but the increases were less when compared to the rats receiving DEN/AAF only.
    Matched MeSH terms: Carcinogens
  20. Robey RB, Weisz J, Kuemmerle NB, Salzberg AC, Berg A, Brown DG, et al.
    Carcinogenesis, 2015 Jun;36 Suppl 1(Suppl 1):S203-31.
    PMID: 26106140 DOI: 10.1093/carcin/bgv037
    Environmental contributions to cancer development are widely accepted, but only a fraction of all pertinent exposures have probably been identified. Traditional toxicological approaches to the problem have largely focused on the effects of individual agents at singular endpoints. As such, they have incompletely addressed both the pro-carcinogenic contributions of environmentally relevant low-dose chemical mixtures and the fact that exposures can influence multiple cancer-associated endpoints over varying timescales. Of these endpoints, dysregulated metabolism is one of the most common and recognizable features of cancer, but its specific roles in exposure-associated cancer development remain poorly understood. Most studies have focused on discrete aspects of cancer metabolism and have incompletely considered both its dynamic integrated nature and the complex controlling influences of substrate availability, external trophic signals and environmental conditions. Emerging high throughput approaches to environmental risk assessment also do not directly address the metabolic causes or consequences of changes in gene expression. As such, there is a compelling need to establish common or complementary frameworks for further exploration that experimentally and conceptually consider the gestalt of cancer metabolism and its causal relationships to both carcinogenesis and the development of other cancer hallmarks. A literature review to identify environmentally relevant exposures unambiguously linked to both cancer development and dysregulated metabolism suggests major gaps in our understanding of exposure-associated carcinogenesis and metabolic reprogramming. Although limited evidence exists to support primary causal roles for metabolism in carcinogenesis, the universality of altered cancer metabolism underscores its fundamental biological importance, and multiple pleiomorphic, even dichotomous, roles for metabolism in promoting, antagonizing or otherwise enabling the development and selection of cancer are suggested.
    Matched MeSH terms: Carcinogens, Environmental/adverse effects*
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