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  1. Fulltext Effect of Air Pollution and Hospital Admission: A Systematic Review
    Ab Manan N, Noor Aizuddin A, Hod R
    Ann Glob Health, 2018 11 05;84(4):670-678.
    PMID: 30779516 DOI: 10.29024/aogh.2376
    IntroductionMany epidemiological studies have demonstrated associations between air pollution levels and human health in terms of hospital admissions. The aim of this paper is to gather evidence concerning air pollution effects on the risk of hospital admission. We hypothesised that increase in: particulate matter (PM), ozone (O3), carbon monoxide (CO), nitrogen dioxide (NO2), and sulphur dioxide (SO2) levels would be associated with the increasing trend of hospital admission.MethodsA systematic review of literature was carried out. Literature search was done in Sage, Ovid Medline, Science Direct, Wiley and ProQuest from 2010 to 2016 using keywords "hospital admission and air pollution". Studies of any relevant design were included if they presented original data, included at least one analysis where hospital admission was the specific outcome, and one or more of the following exposures were investigated: PM, O3, CO, NO2 and SO2.ResultsA total of 175 potential studies were identified by the search. Twenty two studies qualified for the review. Air pollution was noted to have an excessive risk of 3.46 (95%CI, 1.67, 5.27) of total hospital admissions. Cardiovascular admission was noted to have an increased risk of hospitalization for PM2.5 of 1.5 to 2.0; PM10 (1.007 to 2.7); NO2 (1.04 to 1.17) and SO2 (1.007). For respiratory admission, PM2.5 can caused an increased risk of hospitalization by 1.1 to 1.8; PM10 (1.007 to 1.13); NO2 (1.08 to 1.94) and SO2 (1.02). While O3 have minimal effect on COPD and stroke, CO does not influence in the effect of these hospitalization.ConclusionThe exposure to air pollutants confers an increased risk of admission of several disease. Our findings call for greater awareness of environmental protection and the implementation of effective measures to improve the quality of air, which may reduce the risks of adverse effects on the population's health.
    Matched MeSH terms: Environmental Exposure/adverse effects*
  2. Fulltext 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
    Abdul Wahab S, Hassan A, Latif MT, Vadiveel Y, Jeyabalan T, Soo CI, et al.
    Asian Pac J Cancer Prev, 2019 07 01;20(7):1959-1965.
    PMID: 31350951 DOI: 10.31557/APJCP.2019.20.7.1959
    Objective: Epidemiological studies have reported the close relationship between risk for lung cancers and air pollution
    in particular, for non-smoking related lung cancers. However, most studies used residential address as proxies which may
    not estimate accurately an individual’s air pollution exposure. Therefore, the aim of this study was to identify risk factors
    such as occupation and mode of transportation associated with lung cancer diagnosis and death. Methods: Subjects
    with lung cancer (n=514) were evaluated both by chart reviews for clinical data and interviews to determine residential
    address for ten years, main occupation and main mode of transportation. Annual particulate matter with diameter size
    less than 2.5 micrometre (PM2.5) concentration were calculated based on particulate matter with diameter size less than
    10 micrometre (PM10) data recorded by Malaysian Department of Environment. Logistic regression analysis, cluster
    analysis and the Cox regression analysis were performed to the studied variables. Results: This study concurred with
    previous studies that lung adenocarcinoma were 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 (p=0.024). Independent of smoking,
    the κ -means cluster analysis revealed two clusters in which the high risk cluster involves occupation risk with air
    pollution of more than four hours per day, main transportation involving motorcycle and trucks and mean annual PM2.5
    concentration of more than 30 based on residential address for more than ten years. The increased risk for the high-risk
    cluster was more than five times for the diagnosis of lung adenocarcinoma (OR=5.69, 95% CI=3.14-7.21, p<0.001).
    The hazard ratio for the high-risk cluster was 3.89 (95% CI=2.12-4.56, p=0.02) for lung adenocarcinoma mortality at
    1 year. Conclusion: High-risk cluster including PM2.5, occupation risk and mode of transportation as surrogates for
    air-pollution exposure was identified and highly associated with lung adenocarcinoma diagnosis and 1-year mortality.
    Matched MeSH terms: Environmental Exposure/adverse effects*
  3. Associations between air pollutants and peak expiratory flow and fractional exhaled nitric oxide in students
    Adman MA, Hashim JH, Manaf MRA, Norback D
    Int J Tuberc Lung Dis, 2020 02 01;24(2):189-195.
    PMID: 32127103 DOI: 10.5588/ijtld.19.0096
    BACKGROUND: Studies on the effects of outdoor air pollution on the respiratory health of students in tropical countries such as Malaysia are limited.OBJECTIVE: To assess associations between outdoor air pollutants and peak expiratory flow (PEF) and fractional exhaled nitric oxide (FeNO).METHOD: PEF and FeNO levels of 487 students recruited in Melaka and Putrajaya, Malaysia, were measured in April and June 2014. Multiple linear regression with mutual adjustment was used to analyse the associations between exposure to air pollution and health.RESULTS: PEF was significantly associated with ozone for 1-day exposure (β = -13.3 l/min, 95% CI -22.7 to -3.8), carbon monoxide for 2-day exposure (β = -57.2 l/min, 95% CI -90.7 to -23.7) and particulate matter ≦10 μm in diameter for 3-day exposure (β = -6.0 l/min, 95% CI -9.2 to -2.8) and 7-day exposure (β = -8.6 l/min, 95% CI -13.0 to -4.1). Stratified analysis showed that associations between PEF and outdoor air pollutant exposures were similar in students with and without elevated FeNO levels.CONCLUSION: Outdoor air pollution in Malaysia may cause airway obstruction unrelated to eosinophilic airway inflammation among students as measured using FeNO.
    Matched MeSH terms: Environmental Exposure/adverse effects
  4. 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*
  5. 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
  6. Fulltext Long-term exposure to ambient air pollution and incidence of brain tumor: the European Study of Cohorts for Air Pollution Effects (ESCAPE)
    Andersen ZJ, Pedersen M, Weinmayr G, Stafoggia M, Galassi C, Jørgensen JT, et al.
    Neuro-oncology, 2018 02 19;20(3):420-432.
    PMID: 29016987 DOI: 10.1093/neuonc/nox163
    Background: Epidemiological evidence on the association between ambient air pollution and brain tumor risk is sparse and inconsistent.

    Methods: In 12 cohorts from 6 European countries, individual estimates of annual mean air pollution levels at the baseline residence were estimated by standardized land-use regression models developed within the ESCAPE and TRANSPHORM projects: particulate matter (PM) ≤2.5, ≤10, and 2.5-10 μm in diameter (PM2.5, PM10, and PMcoarse), PM2.5 absorbance, nitrogen oxides (NO2 and NOx) and elemental composition of PM. We estimated cohort-specific associations of air pollutant concentrations and traffic intensity with total, malignant, and nonmalignant brain tumor, in separate Cox regression models, adjusting for risk factors, and pooled cohort-specific estimates using random-effects meta-analyses.

    Results: Of 282194 subjects from 12 cohorts, 466 developed malignant brain tumors during 12 years of follow-up. Six of the cohorts also had data on nonmalignant brain tumor, where among 106786 subjects, 366 developed brain tumor: 176 nonmalignant and 190 malignant. We found a positive, statistically nonsignificant association between malignant brain tumor and PM2.5 absorbance (hazard ratio and 95% CI: 1.67; 0.89-3.14 per 10-5/m3), and weak positive or null associations with the other pollutants. Hazard ratio for PM2.5 absorbance (1.01; 0.38-2.71 per 10-5/m3) and all other pollutants were lower for nonmalignant than for malignant brain tumors.

    Conclusion: We found suggestive evidence of an association between long-term exposure to PM2.5 absorbance indicating traffic-related air pollution and malignant brain tumors, and no association with overall or nonmalignant brain tumors.

    Matched MeSH terms: Environmental Exposure/adverse effects*
  7. Fulltext "Care and feeding": the Asian environmental tobacco smoke consultants programme
    Assunta M, Fields N, Knight J, Chapman S
    Tob Control, 2004 Dec;13 Suppl 2:ii4-12.
    PMID: 15564219
    STUDY OBJECTIVE: To review the tobacco industry's Asian environmental tobacco smoke (ETS) consultants programme, focusing on three key nations: China, Hong Kong, and Malaysia.
    METHODS: Systematic keyword and opportunistic website searches of formerly private internal industry documents.
    MAIN RESULTS: The release of the 1986 US Surgeon General's report on second hand smoke provoked tobacco companies to prepare for a major threat to their industry. Asian programme activities included conducting national/international symposiums, consultant "road shows" and extensive lobbying and media activities. The industry exploited confounding factors said to be unique to Asian societies such as diet, culture and urban pollution to downplay the health risks of ETS. The industry consultants were said to be "..prepared to do the kinds of things they were recruited to do".
    CONCLUSIONS: The programme was successful in blurring the science on ETS and keeping the controversy alive both nationally and internationally. For the duration of the project, it also successfully dissuaded national policy makers from instituting comprehensive bans on smoking in public places.
    Matched MeSH terms: Environmental Exposure/adverse effects*
  8. Fulltext Molecular Mechanisms of Stress-Responsive Changes in Collagen and Elastin Networks in Skin
    Aziz J, Shezali H, Radzi Z, Yahya NA, Abu Kassim NH, Czernuszka J, et al.
    Skin Pharmacol Physiol, 2016;29(4):190-203.
    PMID: 27434176 DOI: 10.1159/000447017
    Collagen and elastin networks make up the majority of the extracellular matrix in many organs, such as the skin. The mechanisms which are involved in the maintenance of homeostatic equilibrium of these networks are numerous, involving the regulation of genetic expression, growth factor secretion, signalling pathways, secondary messaging systems, and ion channel activity. However, many factors are capable of disrupting these pathways, which leads to an imbalance of homeostatic equilibrium. Ultimately, this leads to changes in the physical nature of skin, both functionally and cosmetically. Although various factors have been identified, including carcinogenesis, ultraviolet exposure, and mechanical stretching of skin, it was discovered that many of them affect similar components of regulatory pathways, such as fibroblasts, lysyl oxidase, and fibronectin. Additionally, it was discovered that the various regulatory pathways intersect with each other at various stages instead of working independently of each other. This review paper proposes a model which elucidates how these molecular pathways intersect with one another, and how various internal and external factors can disrupt these pathways, ultimately leading to a disruption in collagen and elastin networks.
    Matched MeSH terms: Environmental Exposure/adverse effects
  9. Vitamin E attenuates nicotine- and noise-induced reproductive impairment in male albino Wistar rats
    Bisong SA, Ukoh IE, Nna VU, Ebong PE
    Andrologia, 2018 Sep;50(7):e13050.
    PMID: 29806220 DOI: 10.1111/and.13050
    Previous studies showed that exposure to stress or nicotine induced reproductive impairment in male rats. Here, we assessed the effect of an antioxidant (vitamin E) on nicotine-, stress- and nicotine + stress-induced reproductive impairment in male rats. Forty-eight male albino Wistar rats were divided into eight groups as follows; control, stress (generator noise 90-120 dB, 8 hr/day), nicotine (1.5 mg kg-1 day-1 ), nicotine + stress, vitamin E (100 mg kg-1 day-1 ), stress + vitamin E, nicotine + vitamin E and stress + nicotine + vitamin E. Sperm count, viability, motility and rapid progressive forward movement decreased significantly (p 
    Matched MeSH terms: Environmental Exposure/adverse effects*
  10. 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
  11. Fulltext The effect of environmental chemicals on the tumor microenvironment
    Casey SC, Vaccari M, Al-Mulla F, Al-Temaimi R, Amedei A, Barcellos-Hoff MH, et al.
    Carcinogenesis, 2015 Jun;36 Suppl 1:S160-83.
    PMID: 26106136 DOI: 10.1093/carcin/bgv035
    Potentially carcinogenic compounds may cause cancer through direct DNA damage or through indirect cellular or physiological effects. To study possible carcinogens, the fields of endocrinology, genetics, epigenetics, medicine, environmental health, toxicology, pharmacology and oncology must be considered. Disruptive chemicals may also contribute to multiple stages of tumor development through effects on the tumor microenvironment. In turn, the tumor microenvironment consists of a complex interaction among blood vessels that feed the tumor, the extracellular matrix that provides structural and biochemical support, signaling molecules that send messages and soluble factors such as cytokines. The tumor microenvironment also consists of many host cellular effectors including multipotent stromal cells/mesenchymal stem cells, fibroblasts, endothelial cell precursors, antigen-presenting cells, lymphocytes and innate immune cells. Carcinogens can influence the tumor microenvironment through effects on epithelial cells, the most common origin of cancer, as well as on stromal cells, extracellular matrix components and immune cells. Here, we review how environmental exposures can perturb the tumor microenvironment. We suggest a role for disrupting chemicals such as nickel chloride, Bisphenol A, butyltins, methylmercury and paraquat as well as more traditional carcinogens, such as radiation, and pharmaceuticals, such as diabetes medications, in the disruption of the tumor microenvironment. Further studies interrogating the role of chemicals and their mixtures in dose-dependent effects on the tumor microenvironment could have important general mechanistic implications for the etiology and prevention of tumorigenesis.
    Matched MeSH terms: Environmental Exposure/adverse effects*
  12. Sun exposure and the risk of prostate cancer in the Singapore Prostate Cancer Study: a case-control study
    Chia SE, Wong KY, Cheng C, Lau W, Tan PH
    Asian Pac J Cancer Prev, 2012;13(7):3179-85.
    PMID: 22994730
    BACKGROUND: Most of the epidemiology studies on the effects of sun exposure and prostate cancer were conducted among the temperate countries of North America and Europe. Little is known about the influence on Asian populations. The purpose of current study was to evaluate any association of sun exposure with risk of prostate cancer in Chinese, Malays and Indians who reside in the tropics.

    METHODS: The Singapore Prostate Cancer Study is a hospital-based case-control study of 240 prostate cancer incident cases and 268 controls conducted in Singapore between April 2007 and May 2009. Detailed information on outdoor activities in the sun, skin colour, sun sensitivity and other possible risk factors were collected in personal interviews. Cases were further classified by Gleason scores and TNM staging. Odds ratios (OR) and 95% confidence intervals (CI) were calculated using unconditional logistic regression analysis, adjusted for age, ethnicity, education, family history of any cancers, BMI and skin colour.

    RESULTS: We found that prostate cancer risk was increased in subjects with black/dark-brown eyes (OR 5.88, 95%CI 3.17-10.9), darker skin colour e.g. tan/dark brown/black (OR 7.62, 95%CI 3.41-17.0), frequent sunburn in lifetime (OR 4.30, 95%CI 1.7-11.2) and increased general sun exposure in adulthood per week (OR 2.03, 95%CI 1.09-3.81). The increased risk was consistent for high grade tumours and advanced stage prostate cancers.

    CONCLUSION: The findings from this study suggest that excessive sun exposure is a risk factor for prostate cancer in Asians.

    Matched MeSH terms: Environmental Exposure/adverse effects
  13. 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
  14. 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*
  15. 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
  16. 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*
  17. Polycyclic Aromatic Hydrocarbons (PAHs) and their Bioaccessibility in Meat: a Tool for Assessing Human Cancer Risk
    Hamidi EN, Hajeb P, Selamat J, Abdull Razis AF
    Asian Pac J Cancer Prev, 2016;17(1):15-23.
    PMID: 26838201
    Polycyclic aromatic hydrocarbons (PAHs) are primarily formed as a result of thermal treatment of food, especially barbecuing or grilling. Contamination by PAHs is due to generation by direct pyrolysis of food nutrients and deposition from smoke produced through incomplete combustion of thermal agents. PAHs are ubiquitous compounds, well-known to be carcinogenic, which can reach the food in different ways. As an important human exposure pathway of contaminants, dietary intake of PAHs is of increasing concern for assessing cancer risk in the human body. In addition, the risks associated with consumption of barbecued meat may increase if consumers use cooking practices that enhance the concentrations of contaminants and their bioaccessibility. Since total PAHs always overestimate the actual amount that is available for absorption by the body, bioaccessibility of PAHs is to be preferred. Bioaccessibility of PAHs in food is the fraction of PAHs mobilized from food matrices during gastrointestinal digestion. An in vitro human digestion model was chosen for assessing the bioaccessibility of PAHs in food as it offers a simple, rapid, low cost alternative to human and animal studies; providing insights which may not be achievable in in vivo studies. Thus, this review aimed not only to provide an overview of general aspects of PAHs such as the formation, carcinogenicity, sources, occurrence, and factors affecting PAH concentrations, but also to enhance understanding of bioaccessibility assessment using an in vitro digestion model.
    Matched MeSH terms: Environmental Exposure/adverse effects
  18. Blood lead levels of urban and rural Malaysian primary school children
    Hashim JH, Hashim Z, Omar A, Shamsudin SB
    Asia Pac J Public Health, 2000;12(2):65-70.
    PMID: 11836921
    The objective of this article is to study the influence of exposure and socio-economic variables on the blood lead level of Malaysian school children. Data on respirable lead and blood lead of 346 school children were obtained from Kuala Lumpur (urban), Kemaman (semi-urban) and Setiu (rural). Respirable lead and blood lead were highest for Kuala Lumpur (95 ng/m3 and 5.26 micrograms/dL) followed by Kemaman (27 ng/m3 and 2.81 micrograms/dL) and Setiu (15 ng/m3 and 2.49 micrograms/dL), and the differences were statistically significant. The percentage of school children with excessive blood lead of 10 micrograms/dL or greater was 6.36% overall, and highest for Kuala Lumpur (11.73%). Regression analyses show that urban children are at higher risk of exhibiting excessive blood lead levels. Kuala Lumpur's school children have a 25 times greater risk of having excessive blood lead levels when compared to Kemaman's and Setiu's school children. Respirable and blood lead were correlated (r = 0.999, p = 0.021). Urban school children acquire higher blood lead levels than their rural and semi-urban counterparts, even after controlling for age, sex, parents' education and income levels. In conclusion, it is time that lead in the Malaysian environment and population be monitored closely, especially its temporal and spatial variability. Only then can a comprehensive preventive strategy be implemented.
    Matched MeSH terms: Environmental Exposure/adverse effects
  19. Parental awareness and attitude towards environmental tobacco smoke exposure in children with respiratory illnesses
    Hasniah AL, Tan YP, Nur Buhairah MA, Chan TW, Muhammad Nabil TI, Syed Zulkifli SZ
    Public Health, 2016 08;137:182-4.
    PMID: 26976490 DOI: 10.1016/j.puhe.2015.10.028
    Matched MeSH terms: Environmental Exposure/adverse effects*
  20. Lead exposure in the lead-acid storage battery manufacturing and PVC compounding industries
    Ho SF, Sam CT, Embi GB
    Occup Med (Lond), 1998 Sep;48(6):369-73.
    PMID: 10024732
    This study was conducted as part of the Human Exposure Assessment Location (HEAL) Project which comes under the United Nations Environment Programme/World Health Organisation (UNEP/WHO) Global environmental Monitoring System (GEMS). The objective of the study was to evaluate workers' exposure to lead in industries with the highest exposure. All subjects were interviewed about their occupational and smoking histories, the use of personal protective equipment and personal hygiene. The contribution of a dietary source of lead intake from specified foods known to contain lead locally and personal air sampling for lead were assessed. A total of 61 workers from two PVC compounding and 50 workers from two lead acid battery manufacturing plants were studied together with 111 matched controls. In the PVC compounding plants the mean lead-in-air level was 0.0357 mg/m3, with the highest levels occurring during the pouring and mixing operations. This was lower than the mean lead-in-air level of 0.0886 mg/m3 in the lead battery manufacturing plants where the highest exposure was in the loading of lead ingots into milling machines. Workers in lead battery manufacturing had significantly higher mean blood lead than the PVC workers (means, 32.51 and 23.91 mcg/100 ml respectively), but there was poor correlation with lead-in-air levels. Among the lead workers, the Malays had significantly higher blood lead levels than the Chinese (mean blood levels were 33.03 and 25.35 mcg/100 ml respectively) although there was no significant difference between the two ethnic groups in the control group. There were no significant differences between the exposed and control group in terms of dietary intake of specified local foods known to contain lead. However, Malays consumed significantly more fish than the Chinese did. There were no ethnic differences in the hours of overtime work, number of years of exposure, usage of gloves and respirators and smoking habits. Among the Malays, 94.3% eat with their hands compared with 9.2% of the Chinese. Workers who ate with bare hands at least once a week had higher blood lead levels after adjusting for lead-in-air levels (mean blood lead was 30.2 and 26.4 mcg/100 ml respectively). The study indicated that the higher blood lead levels observed in the Malay workers might have been due to their higher exposure and eating with bare hands.
    Matched MeSH terms: Environmental Exposure/adverse effects
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