Displaying publications 21 - 40 of 55 in total

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  1. Fulltext Mechanisms of environmental chemicals that enable the cancer hallmark of evasion of growth suppression
    Nahta R, Al-Mulla F, Al-Temaimi R, Amedei A, Andrade-Vieira R, Bay SN, et al.
    Carcinogenesis, 2015 Jun;36 Suppl 1:S2-18.
    PMID: 26106139 DOI: 10.1093/carcin/bgv028
    As part of the Halifax Project, this review brings attention to the potential effects of environmental chemicals on important molecular and cellular regulators of the cancer hallmark of evading growth suppression. Specifically, we review the mechanisms by which cancer cells escape the growth-inhibitory signals of p53, retinoblastoma protein, transforming growth factor-beta, gap junctions and contact inhibition. We discuss the effects of selected environmental chemicals on these mechanisms of growth inhibition and cross-reference the effects of these chemicals in other classical cancer hallmarks.
    Matched MeSH terms: Environmental Exposure/adverse effects*
  2. Fulltext The impact of low-dose carcinogens and environmental disruptors on tissue invasion and metastasis
    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: Environmental Exposure/adverse effects
  3. Fulltext The potential for chemical mixtures from the environment to enable the cancer hallmark of sustained proliferative signalling
    Engström W, Darbre P, Eriksson S, Gulliver L, Hultman T, Karamouzis MV, et al.
    Carcinogenesis, 2015 Jun;36 Suppl 1:S38-60.
    PMID: 26106143 DOI: 10.1093/carcin/bgv030
    The aim of this work is to review current knowledge relating the established cancer hallmark, sustained cell proliferation to the existence of chemicals present as low dose mixtures in the environment. Normal cell proliferation is under tight control, i.e. cells respond to a signal to proliferate, and although most cells continue to proliferate into adult life, the multiplication ceases once the stimulatory signal disappears or if the cells are exposed to growth inhibitory signals. Under such circumstances, normal cells remain quiescent until they are stimulated to resume further proliferation. In contrast, tumour cells are unable to halt proliferation, either when subjected to growth inhibitory signals or in the absence of growth stimulatory signals. Environmental chemicals with carcinogenic potential may cause sustained cell proliferation by interfering with some cell proliferation control mechanisms committing cells to an indefinite proliferative span.
    Matched MeSH terms: Environmental Exposure/adverse effects*
  4. Fulltext Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: the challenge ahead
    Goodson WH, Lowe L, Carpenter DO, Gilbertson M, Manaf Ali A, Lopez de Cerain Salsamendi A, et al.
    Carcinogenesis, 2015 Jun;36 Suppl 1:S254-96.
    PMID: 26106142 DOI: 10.1093/carcin/bgv039
    Lifestyle factors are responsible for a considerable portion of cancer incidence worldwide, but credible estimates from the World Health Organization and the International Agency for Research on Cancer (IARC) suggest that the fraction of cancers attributable to toxic environmental exposures is between 7% and 19%. To explore the hypothesis that low-dose exposures to mixtures of chemicals in the environment may be combining to contribute to environmental carcinogenesis, we reviewed 11 hallmark phenotypes of cancer, multiple priority target sites for disruption in each area and prototypical chemical disruptors for all targets, this included dose-response characterizations, evidence of low-dose effects and cross-hallmark effects for all targets and chemicals. In total, 85 examples of chemicals were reviewed for actions on key pathways/mechanisms related to carcinogenesis. Only 15% (13/85) were found to have evidence of a dose-response threshold, whereas 59% (50/85) exerted low-dose effects. No dose-response information was found for the remaining 26% (22/85). Our analysis suggests that the cumulative effects of individual (non-carcinogenic) chemicals acting on different pathways, and a variety of related systems, organs, tissues and cells could plausibly conspire to produce carcinogenic synergies. Additional basic research on carcinogenesis and research focused on low-dose effects of chemical mixtures needs to be rigorously pursued before the merits of this hypothesis can be further advanced. However, the structure of the World Health Organization International Programme on Chemical Safety 'Mode of Action' framework should be revisited as it has inherent weaknesses that are not fully aligned with our current understanding of cancer biology.
    Matched MeSH terms: Environmental Exposure/adverse effects*
  5. Fulltext Metabolic reprogramming and dysregulated metabolism: cause, consequence and/or enabler of environmental carcinogenesis?
    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: Environmental Exposure/adverse effects*
  6. Fulltext Disruptive chemicals, senescence and immortality
    Carnero A, Blanco-Aparicio C, Kondoh H, Lleonart ME, Martinez-Leal JF, Mondello C, et al.
    Carcinogenesis, 2015 Jun;36 Suppl 1(Suppl 1):S19-37.
    PMID: 26106138 DOI: 10.1093/carcin/bgv029
    Carcinogenesis is thought to be a multistep process, with clonal evolution playing a central role in the process. Clonal evolution involves the repeated 'selection and succession' of rare variant cells that acquire a growth advantage over the remaining cell population through the acquisition of 'driver mutations' enabling a selective advantage in a particular micro-environment. Clonal selection is the driving force behind tumorigenesis and possesses three basic requirements: (i) effective competitive proliferation of the variant clone when compared with its neighboring cells, (ii) acquisition of an indefinite capacity for self-renewal, and (iii) establishment of sufficiently high levels of genetic and epigenetic variability to permit the emergence of rare variants. However, several questions regarding the process of clonal evolution remain. Which cellular processes initiate carcinogenesis in the first place? To what extent are environmental carcinogens responsible for the initiation of clonal evolution? What are the roles of genotoxic and non-genotoxic carcinogens in carcinogenesis? What are the underlying mechanisms responsible for chemical carcinogen-induced cellular immortality? Here, we explore the possible mechanisms of cellular immortalization, the contribution of immortalization to tumorigenesis and the mechanisms by which chemical carcinogens may contribute to these processes.
    Matched MeSH terms: Environmental Exposure/adverse effects
  7. Risk of concentrations of major air pollutants on the prevalence of cardiovascular and respiratory diseases in urbanized area of Kuala Lumpur, Malaysia
    Tajudin MABA, Khan MF, Mahiyuddin WRW, Hod R, Latif MT, Hamid AH, et al.
    Ecotoxicol Environ Saf, 2019 Apr 30;171:290-300.
    PMID: 30612017 DOI: 10.1016/j.ecoenv.2018.12.057
    Rapid urbanisation in Malaysian cities poses risks to the health of residents. This study aims to estimate the relative risk (RR) of major air pollutants on cardiovascular and respiratory hospitalisations in Kuala Lumpur. Daily hospitalisations due to cardiovascular and respiratory diseases from 2010 to 2014 were obtained from the Hospital Canselor Tuanku Muhriz (HCTM). The trace gases, PM10 and weather variables were obtained from the Department of Environment (DOE) Malaysia in consistent with the hospitalisation data. The RR was estimated using a Generalised Additive Model (GAM) based on Poisson regression. A "lag" concept was used where the analysis was segregated into risks of immediate exposure (lag 0) until exposure after 5 days (lag 5). The results showed that the gases could pose significant risks towards cardiovascular and respiratory hospitalisations. However, the RR value of PM10 was not significant in this study. Immediate effects on cardiovascular hospitalisations were observed for NO2 and O3 but no immediate effect was found on respiratory hospitalisations. Delayed effects on cardiovascular and respiratory hospitalisations were found with SO2 and NO2. The highest RR value was observed at lag 4 for respiratory admissions with SO2 (RR = 1.123, 95% CI = 1.045-1.207), followed by NO2 at lag 5 for cardiovascular admissions (RR = 1.025, 95% CI = 1.005-1.046). For the multi-pollutant model, NO2 at lag 5 showed the highest risks towards cardiovascular hospitalisations after controlling for O3 8 h mean lag 1 (RR = 1.026, 95% CI = 1.006-1.047), while SO2 at lag 4 showed highest risks towards respiratory hospitalisations after controlling for NO2 lag 3 (RR = 1.132, 95% CI = 1.053-1.216). This study indicated that exposure to trace gases in Kuala Lumpur could lead to both immediate and delayed effects on cardiovascular and respiratory hospitalisations.
    Matched MeSH terms: Environmental Exposure/adverse effects*
  8. Fulltext Public perception on human exposure risk: A case study on endocrine disrupting compounds in the environment
    Wee SY, Aris AZ, Yusoff FM, Praveena SM
    Ecotoxicol Environ Saf, 2024 Jan 15;270:115830.
    PMID: 38141339 DOI: 10.1016/j.ecoenv.2023.115830
    Humans are exposed to environmental risks owing to the broad usage of endocrine disrupting compounds (EDCs). However, the subjective evaluation of risk levels and characteristics, as well as the variation in risk processing, have not been thoroughly examined. The objective was to understand the public's perception of the risk associated with human exposure to environmental EDCs and identify any variations in risk perception. In this pioneering study conducted within the distinctive social and cultural context of Malaysia, a developing nation, a quantitative analysis approach was employed to assess the subjective evaluation of risk levels and characteristics among the public while developing a risk perception model. Data gathered from surveys and questionnaires were analyzed to gather information on the public's perception of environmental and health issues pertaining to pesticides, hormones, plastics, medicines, and cosmetics. The analysis revealed that the majority of the public assessed the level of human exposure to environmental risks based on experiential processing, which was influenced by cognitive and affective variables. Interestingly, a higher proportion of individuals in the community had a low risk perception of environmental EDCs, surpassing the overall risk perception by 19.3%. Furthermore, the public showed significant awareness of environmental and health issues related to pesticides, hormones, and plastics but had a lesser inclination to acknowledge the vulnerability of humans to risks associated with medicines and cosmetics. These findings suggest that the public is likely to be exposed to environmental EDCs based on their current perceived risks, and that sociopsychological factors play a significant role in shaping perceptions and judgments. This understanding can inform the development of targeted risk management strategies and interventions to mitigate the potential harm caused by environmental EDCs.
    Matched MeSH terms: Environmental Exposure/adverse effects
  9. Assessment of health risks and individuals' willingness to participate in drinking water management at flood-prone Pahang River Basin, Malaysia
    Alam L, Rahman LF, Ahmed MF, Bari MA, Masud MM, Mokhtar MB
    Environ Geochem Health, 2021 May;43(5):2049-2063.
    PMID: 33389458 DOI: 10.1007/s10653-020-00783-0
    Rivers, the main source of the domestic water supply in Malaysia, have been threatened by frequent flooding in recent years. This study aims to assess human health risks associated with exposure to concentrated heavy metals in a flood-prone region of Malaysia and investigate the affected individuals' willingness to participate in managing water resources. Hazard indices and cancer risks associated with water contamination by heavy metals have been assessed following the method prescribed by the US Environmental Protection Agency. Yearly data of heavy metal contamination (Cd, Cr, Pb, Zn, Fe), water quality parameters (DO, BOD, COD, pH), and climatic information (annual rainfall, annual temperature) have been collected from the Department of Environment and Meteorological Department of Malaysia, respectively. The inductively coupled plasma mass spectrometry technique has been used by the department of environment for analyzing heavy metal concentration in river water samples. In this study, data from a stratified random sample of households in the affected region were analyzed, using partial least squares structural equation modeling, to predict the link between individuals' perceptions and attitudes about water resources and their willingness to engage in water management program. The health risk estimation indicated that the hazard index values were below the acceptable limit, representing no non-carcinogenic risk to adults and children residing in the study area via oral intake and dermal adsorption of water. However, the calculated value for cancer risk signified possible carcinogenic risks associated with Pb and Cd. In general, contamination due to pollution and flooding tends to increase in the basin region, and appropriate management is needed. The results identified perceived water quality as a significant factor influencing people's attitudes toward involvement in water management programs. As in many developing countries, there is no legal provision guaranteeing public representation in water management in Malaysia. The conclusion discusses the importance of these for the literature and for informing future policy actions.
    Matched MeSH terms: Environmental Exposure/adverse effects
  10. Exposure assessment for trace elements from consumption of marine fish in Southeast Asia
    Agusa T, Kunito T, Sudaryanto A, Monirith I, Kan-Atireklap S, Iwata H, et al.
    Environ Pollut, 2007 Feb;145(3):766-77.
    PMID: 16828209
    Concentrations of 20 trace elements were determined in muscle and liver of 34 species of marine fish collected from coastal areas of Cambodia, Indonesia, Malaysia and Thailand. Large regional difference was observed in the levels of trace elements in liver of one fish family (Carangidae): the highest mean concentration was observed in fish from the Malaysian coastal waters for V, Cr, Zn, Pb and Bi and those from the Java Sea side of Indonesia for Sn and Hg. To assess the health risk to the Southeast Asian populations from consumption of fish, intake rates of trace elements were estimated. Some marine fish showed Hg levels higher than the guideline values by U.S. Environmental Protection Agency and Joint FAO/WHO Expert Committee on Food Additives (JECFA). This suggests that consumption of these fish may be hazardous to the people.
    Matched MeSH terms: Environmental Exposure/adverse effects*
  11. Heavy metal quantification of classroom dust in school environment and its impacts on children health from Rawang (Malaysia)
    Tan SY, Praveena SM, Abidin EZ, Cheema MS
    Environ Sci Pollut Res Int, 2018 Dec;25(34):34623-34635.
    PMID: 30315534 DOI: 10.1007/s11356-018-3396-x
    This study aimed to determine bioavailable heavy metal concentrations (As, Cd, Co, Cu, Cr, Ni, Pb, Zn) and their potential sources in classroom dust collected from children's hand palms in Rawang (Malaysia). This study also aimed to determine the association between bioavailable heavy metal concentration in classroom dust and children's respiratory symptoms. Health risk assessment (HRA) was applied to evaluate health risks (non-carcinogenic and carcinogenic) due to heavy metals in classroom dust. The mean of bioavailable heavy metal concentrations in classroom dust found on children's hand palms was shown in the following order: Zn (1.25E + 01 μg/g) > Cu (9.59E-01 μg/g) > Ni (5.34E-01 μg/g) > Cr (4.72E-02 μg/g) > Co (2.34E-02 μg/g) > As (1.77E-02 μg/g) > Cd (9.60E-03 μg/g) > Pb (5.00E-03 μg/g). Hierarchical cluster analysis has clustered 17 sampling locations into three clusters, whereby cluster 1 (S3, S4, S6, S15) located in residential areas and near to roads exposed to vehicle emissions, cluster 2 (S10, S12, S9, S7) located near Rawang town and cluster 3 (S13, S16, S1, S2, S8, S14, S11, S17, S5) located near industrial, residential and plantation areas. Emissions from vehicles, plantations and industrial activities were found as the main sources of heavy metals in classroom dust in Rawang. There is no association found between bioavailable heavy metal concentrations and respiratory symptoms, except for Cu (OR = 0.03). Health risks (non-carcinogenic and carcinogenic risks) indicated that there are no potential non-carcinogenic and carcinogenic risks of heavy metals in classroom dust toward children health.
    Matched MeSH terms: Environmental Exposure/adverse effects
  12. Fuzzy logic and adaptive neuro-fuzzy inference system for characterization of contaminant exposure through selected biomarkers in African catfish
    Karami A, Keiter S, Hollert H, Courtenay SC
    Environ Sci Pollut Res Int, 2013 Mar;20(3):1586-95.
    PMID: 22752811 DOI: 10.1007/s11356-012-1027-5
    This study represents a first attempt at applying a fuzzy inference system (FIS) and an adaptive neuro-fuzzy inference system (ANFIS) to the field of aquatic biomonitoring for classification of the dosage and time of benzo[a]pyrene (BaP) injection through selected biomarkers in African catfish (Clarias gariepinus). Fish were injected either intramuscularly (i.m.) or intraperitoneally (i.p.) with BaP. Hepatic glutathione S-transferase (GST) activities, relative visceral fat weights (LSI), and four biliary fluorescent aromatic compounds (FACs) concentrations were used as the inputs in the modeling study. Contradictory rules in FIS and ANFIS models appeared after conversion of bioassay results into human language (rule-based system). A "data trimming" approach was proposed to eliminate the conflicts prior to fuzzification. However, the model produced was relevant only to relatively low exposures to BaP, especially through the i.m. route of exposure. Furthermore, sensitivity analysis was unable to raise the classification rate to an acceptable level. In conclusion, FIS and ANFIS models have limited applications in the field of fish biomarker studies.
    Matched MeSH terms: Environmental Exposure/adverse effects*
  13. Fulltext How does exposure to pesticides vary in space and time for residents living near to treated orchards?
    Wong HL, Garthwaite DG, Ramwell CT, Brown CD
    Environ Sci Pollut Res Int, 2017 Dec;24(34):26444-26461.
    PMID: 28948535 DOI: 10.1007/s11356-017-0064-5
    This study investigated changes over 25 years (1987-2012) in pesticide usage in orchards in England and Wales and associated changes to exposure and risk for resident pregnant women living 100 and 1000 m downwind of treated areas. A model was developed to estimate aggregated daily exposure to pesticides via inhaled vapour and indirect dermal contact with contaminated ground, whilst risk was expressed as a hazard quotient (HQ) based on estimated exposure and the no observed (adverse) effect level for reproductive and developmental effects. Results show the largest changes occurred between 1987 and 1996 with total pesticide usage reduced by ca. 25%, exposure per unit of pesticide applied slightly increased, and a reduction in risk per unit exposure by factors of 1.3 to 3. Thereafter, there were no consistent changes in use between 1996 and 2012, with an increase in number of applications to each crop balanced by a decrease in average application rate. Exposure per unit of pesticide applied decreased consistently over this period such that values in 2012 for this metric were 48-65% of those in 1987, and there were further smaller decreases in risk per unit exposure. All aggregated hazard quotients were two to three orders of magnitude smaller than one, despite the inherent simplifications of assuming co-occurrence of exposure to all pesticides and additivity of effects. Hazard quotients at 1000 m were 5 to 16 times smaller than those at 100 m. There were clear signals of the impact of regulatory intervention in improving the fate and hazard profiles of pesticides used in orchards in England and Wales over the period investigated.
    Matched MeSH terms: Environmental Exposure/adverse effects*
  14. Bisphenol A and its effects on the systemic organs of children
    Zulkifli S, Rahman AA, Kadir SHSA, Nor NSM
    Eur J Pediatr, 2021 Oct;180(10):3111-3127.
    PMID: 33893858 DOI: 10.1007/s00431-021-04085-0
    For the past two decades, growing research has been pointing to multiple repercussions of bisphenol A (BPA) exposure to human health. BPA is a synthetic oestrogen which primarily targets the endocrine system; however, the compound also disturbs other systemic organ functions, in which the magnitude of impacts in those other systems is as comparable to those in the endocrine system. To date, the discoveries on the association between BPA and health outcomes mainly came from animal and in vitro studies, with limited human studies which emphasised on children's health. In this comprehensive review, we summarised studies on human, in vivo and in vitro models to understand the consequences of pre-, post- and perinatal BPA exposure on the perinatal, children and adult health, encompassing cardiovascular, neurodevelopmental, endocrine and reproductive effects.Conclusion: Evidence from in vitro and animal studies may provide further support and better understanding on the correlation between environmental BPA exposure and its detrimental effects in humans and child development, despite the difficulties to draw direct causal relations of BPA effects on the pathophysiology of the diseases/syndromes in children, due to differences in body system complexity between children and adults, as well as between animal and in vitro models and humans. What is known: • Very limited reviews are available on how BPA adversely affects children's health. • Previous papers mainly covered two systems in children. What is new: • Comprehensive review on the detrimental effects of BPA on children health outcomes, including expectations on adult health outcomes following perinatal BPA exposure, as well as covering a small part of BPA alternatives. • Essentially, BPA exposure during pregnancy has huge impacts on the foetus in which it may cause changes in foetal epigenetic programming, resulting in disease onsets during childhood as well as adulthood.
    Matched MeSH terms: Environmental Exposure/adverse effects
  15. Is There an Association Between Ambient Air Pollution and Bladder Cancer Incidence? Analysis of 15 European Cohorts
    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: Environmental Exposure/adverse effects*
  16. Dietary intake of aflatoxins in the adult Malaysian population - an assessment of risk
    Chin CK, Abdullah A, Sugita-Konishi Y
    Food Addit Contam Part B Surveill, 2012;5(4):286-94.
    PMID: 24786411 DOI: 10.1080/19393210.2012.713028
    Exposure to aflatoxins in the adult Malaysian diet was estimated by analysing aflatoxins in 236 food composites prepared as "ready for consumption". Dietary exposure to aflatoxin B1 (AFB1) ranged from 24.3 to 34.00 ng/kg b.w./day (lower to upper bound), with peanuts being the main contributor. Estimated liver cancer risk from this exposure was 0.61-0.85 cancers/100,000 population/year, contributing 12.4%-17.3% of the liver cancer cases. Excluding AFB1 occurrence data higher than 15 µg/kg reduced exposure by 65%-91% to 2.27-11.99 ng/kg b.w./day, reducing the cancer risk to 0.06-0.30 cancers/100,000 population/year (contributing 1.2%-6.1% liver cancer cases). Reducing further the ML of AFB1 from 15 to 5 µg/kg yielded 3%-7% greater drop in the exposure to 0.47-10.26 ng/kg b.w./day with an estimated risk of 0.01-0.26 cancers/100,000 population/year (0.2%-5.1% liver cancer cases attributed to dietary AFB1). These findings indicate that current MLs are adequate in protecting Malaysians' health.
    Matched MeSH terms: Environmental Exposure/adverse effects
  17. Environmental contamination in the hospital as a possible source for nosocomial infection with methicillin-resistant Staphylococcus aureus
    Ghaznavi-Rad E, Ghasemzadeh-Moghaddam H, Shamsudin MN, Hamat RA, Sekawi Z, Aziz MN, et al.
    Infect Control Hosp Epidemiol, 2010 Dec;31(12):1302-3.
    PMID: 21028965 DOI: 10.1086/657587
    Matched MeSH terms: Environmental Exposure/adverse effects
  18. The impact of traffic-related air pollution on lung function status and respiratory symptoms among children in Klang Valley, Malaysia
    Suhaimi NF, Jalaludin J, Mohd Juhari MA
    Int J Environ Health Res, 2022 Mar;32(3):535-546.
    PMID: 32579034 DOI: 10.1080/09603123.2020.1784397
    Increasing the range of vehicles on traffic roads in the urban area has led to traffic-related air pollution (TRAP) and is currently becoming the main concern for health, especially among children. The study aimed to determine associations between TRAP and respiratory health, also to identify the main factors that influenced them. A cross-sectional comparative study was carried out among children in high and low traffic areas. Air quality monitoring was conducted in six primary schools. A set of standardized questionnaires was distributed to obtain respondents' exposure history and respiratory health symptoms, while spirometry test was carried out to determine the lung function status. There were associations between TRAP and abnormality of FEV1% among children. NO2 was the main predictor that influenced both chest tightness and abnormality of FEV1%. Children exposed to a high level of traffic-related air pollution have an increased risk of respiratory symptoms and abnormality of lung function.
    Matched MeSH terms: Environmental Exposure/adverse effects
  19. Exploring cancer development in adulthood: cholinesterase depression and genotoxic effect from chronic exposure to organophosphate pesticides among rural farm children
    How V, Hashim Z, Ismail P, Md Said S, Omar D, Bahri Mohd Tamrin S
    J Agromedicine, 2014;19(1):35-43.
    PMID: 24417530 DOI: 10.1080/1059924X.2013.866917
    Children are the vulnerable group in the agricultural community due to their early exposure to pesticides through the dynamic interplay between genetic predisposition, environment, and host-related factors. This study aims to identify the possible association between the depression in blood cholinesterase level and genotoxic effect among farm children. The results of micronuclei assay and comet assay showed that the reduced blood cholinesterase level from organophosphate pesticide exposure is significantly associated with an increase in chromosome breakage and DNA strand breaks. These genotoxicity end points suggest that farm children's cells experience early DNA damage that may lead to uncontrolled cell proliferation during their adulthood. Thus, farm children who grow up near pesticide-treated farmland have a higher probability of developing cancer than children with minimal or zero exposure to pesticides.
    Matched MeSH terms: Environmental Exposure/adverse effects*
  20. Tuning into the travel health risks of music tourism
    Lu TS, Flaherty GT
    J Travel Med, 2018 01 01;25(1).
    PMID: 30346571 DOI: 10.1093/jtm/tay106
    Matched MeSH terms: Environmental Exposure/adverse effects*
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