Displaying publications 21 - 40 of 56 in total

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  1. Tan SH, Karri V, Tay NWR, Chang KH, Ah HY, Ng PQ, et al.
    Biomed Pharmacother, 2019 Mar;111:765-777.
    PMID: 30612001 DOI: 10.1016/j.biopha.2018.12.101
    Neurodegenerative diseases are usually sporadic in nature and commonly influenced by a wide range of genetic, life style and environmental factors. A unifying feature of Alzheimer's disease (AD) and Parkinson's disease (PD) is the abnormal accumulation and processing of mutant or damaged intra and extracellular proteins; this leads to neuronal vulnerability and dysfunction in the brain. Through a detailed review of ubiquitin proteasome, mRNA splicing, mitochondrial dysfunction, and oxidative stress pathway interrelation on neurodegeneration can improve the understanding of the disease mechanism. The identified pathways common to AD and PD nominate promising new targets for further studies, and as well as biomarkers. These insights suggested would likely provide major stimuli for developing unified treatment approaches to combat neurodegeneration. More broadly, pathways can serve as vehicles for integrating findings from diverse studies of neurodegeneration. The evidence examined in this review provides a brief overview of the current literature on significant pathways in promoting in AD, PD. Additionally, these insights suggest that biomarkers and treatment strategies may require simultaneous targeting of multiple components.
    Matched MeSH terms: Environmental Exposure/adverse effects*
  2. Idris IB, Ghazi HF, Zhie KH, Khairuman KA, Yahya SK, Abd Zaim FA, et al.
    Ann Glob Health, 2016 6 22;82(1):202-8.
    PMID: 27325078 DOI: 10.1016/j.aogh.2016.01.021
    The prevalence of asthma is increasing, especially among children in Malaysia, with environmental factors as one of the main preventable contributors. The aim of this study was to determine the association between environmental air pollutants and the occurrence of asthma among children seen in pediatric clinics in Universiti Kebangsaan Malaysia Medical Center (UKMMC), Kuala Lumpur. An unmatched case control study among children who attended the pediatric clinic was carried out from May to August 2015. A total of 223 children who were diagnosed with asthma (105 cases) and who did not have asthma (118 controls) were included in this study. Their parents or caregivers were interviewed using questionnaires modified from the International Study of Asthma and Allergies in Childhood. Data obtained were analyzed using SPSS software version 20. There was a higher risk of asthma in those who had carpet at home (OR = 2.15 CI [1.25-3.68]), those who lived within 200 m of heavy traffic (OR = 1.72 CI [1.01-2.93]), and those who were exposed to lorry fumes (OR = 2.61. CI [1.38-4.93]). Environmental air pollutants increased the risk of asthma among children in Malaysia. Exposure to congested roads, lorry fumes, and indoor carpet were associated with asthma among children in this study. Parents or caretakers of children with asthma should be given adequate education on the prevention of asthmatic attack among these children.
    Study site: Paediatric clinic, Pusat Perubatan Universiti Kebangsaan Malaysia (PPUKM), Kuala Lumpur, Malaysia
    Matched MeSH terms: Environmental Exposure/adverse effects*
  3. 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
  4. Thompson PA, Khatami M, Baglole CJ, Sun J, Harris SA, Moon EY, et al.
    Carcinogenesis, 2015 Jun;36 Suppl 1:S232-53.
    PMID: 26106141 DOI: 10.1093/carcin/bgv038
    An emerging area in environmental toxicology is the role that chemicals and chemical mixtures have on the cells of the human immune system. This is an important area of research that has been most widely pursued in relation to autoimmune diseases and allergy/asthma as opposed to cancer causation. This is despite the well-recognized role that innate and adaptive immunity play as essential factors in tumorigenesis. Here, we review the role that the innate immune cells of inflammatory responses play in tumorigenesis. Focus is placed on the molecules and pathways that have been mechanistically linked with tumor-associated inflammation. Within the context of chemically induced disturbances in immune function as co-factors in carcinogenesis, the evidence linking environmental toxicant exposures with perturbation in the balance between pro- and anti-inflammatory responses is reviewed. Reported effects of bisphenol A, atrazine, phthalates and other common toxicants on molecular and cellular targets involved in tumor-associated inflammation (e.g. cyclooxygenase/prostaglandin E2, nuclear factor kappa B, nitric oxide synthesis, cytokines and chemokines) are presented as example chemically mediated target molecule perturbations relevant to cancer. Commentary on areas of additional research including the need for innovation and integration of systems biology approaches to the study of environmental exposures and cancer causation are presented.
    Matched MeSH terms: Environmental Exposure/adverse effects*
  5. 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*
  6. 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*
  7. 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*
  8. 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
  9. 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*
  10. 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*
  11. 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
  12. 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*
  13. 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*
  14. 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*
  15. 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
  16. 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*
  17. Junus S, Chew CC, Sugunan P, Meor-Aziz NF, Zainal NA, Hassan HM, et al.
    BMC Public Health, 2021 10 15;21(1):1860.
    PMID: 34654405 DOI: 10.1186/s12889-021-11825-2
    BACKGROUND: Secondhand smoke (SHS) exposure can affect physical development in children. An understanding of parental risk perception of SHS could guide efforts to develop measures for prevention of SHS exposure among children. This study aimed to assess parental risk perceptions of SHS and action taken by parents to minimise SHS exposure in their children.

    METHODS: This cross-sectional nationwide study conducted in 2018 recruited convenience sample of 289 parents with children up to age 12 at public areas. Parents were asked to rate the risk level from 1 (no risk) to 5 (extremely high risk) by looking at photographs of an adult smoking in the presence of a child in 8 different situations. The implementation of smoking restriction rules was assessed. Mean scores were calculated with higher scores representing higher risk perception of SHS to child's health. Linear regression analysis was used to determine factors associated with the level of parental risk perception of SHS exposure to their children's health.

    RESULTS: A total of 246 parents responded. Their mean age was 35 years (SD 6.4). The majority were mothers (75.6%), Malays (72.0%) and had tertiary education level (82.5%), and non-smoker (87.1%). The mean age of respondents' youngest child was 3 years (SD 3.1). The risk perception level was high [mean scores: 4.11 (SD: 0.82)]. Most parents implemented household (65.0%) and car (68.3%) smoking restriction rules. Lower levels of risk perception were observed among participants who were current smokers (p 

    Matched MeSH terms: Environmental Exposure/adverse effects
  18. Ramli R, Che Man Z, Nordin R, Abdul Karim F, Rashdi MF, Oxley J, et al.
    Traffic Inj Prev, 2016 Sep;17 Suppl 1:79-85.
    PMID: 27586107 DOI: 10.1080/15389588.2016.1203428
    OBJECTIVE: Vietnamese spend hours travelling on the road using their motorcycles. Their helmets are exposed continuously to sunlight and rain. The objectives of this study were to determine the association between the effect of photo-oxidative degradation (POD) of the outer shells and helmet age on helmet damage. The micro-structural change of the outer shell was also investigated.

    METHODS: This was a prospective, cross sectional study recruiting injured motorcyclists from Hanoi, Vietnam hospital. The participants were interviewed by a trained researcher. The participants' helmets were collected post-crash. Initially, the helmets were examined for their type and external characteristics. A 3 cm × 3 cm cut was made on the helmet in the impacted and non-impacted areas (control). These areas were investigated for evidence of POD and presence of micro-cracks and material disintegration. 50 participants were enrolled. Sources of information included questionnaire and laboratory analyses. The helmet factors of interest were age of the helmet, exposure of helmet to sunlight and rain (duration/day) and history of previous impact. Laboratory analyses included Fourier Transform Infra Red (FTIR) for degradation and scanning electron microscopy (SEM) for micro-structural examination.

    RESULTS: Majority of the helmets was the open-face type, 40 (80.0%). 31 (62.0%) helmets aged less than three years (LTY) and 19 (38.0%) were three years old or more (MTY). 19 (61.3%) of the LTY helmets and 12 (63.2%) MTY helmets showed evidence of POD. The duration of helmet exposure to sunlight was between 93 to 6570 hours (mean 2347.74 hours; SD 1733.39). The SEM showed 15 helmets (30%) with micro-fractures, 21 helmets (42.0%) with material disintegration. Prolonged uv exposure to the ABS helmets resulted in changes in the helmet material in the form of material disintegration and microcracks and this association was statistically significant (p = 0.03).

    CONCLUSION: POD occurs due to routine exposure to the ultraviolet light. Prolonged uv exposure affects outer shell surface material integrity.

    Matched MeSH terms: Environmental Exposure/adverse effects*
  19. 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
  20. 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
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