Displaying publications 1 - 20 of 55 in total

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  1. Moritz KB, Kopp T, Stingl G, Bublin M, Breiteneder H, Wöhrl S
    Allergol Immunopathol (Madr), 2011 Jul-Aug;39(4):244-5.
    PMID: 21741147 DOI: 10.1016/j.aller.2010.06.010
    Matched MeSH terms: Environmental Exposure/adverse effects
  2. 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*
  3. 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*
  4. 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*
  5. Ong LC, Chung FF, Tan YF, Leong CO
    Arch Toxicol, 2016 Jan;90(1):103-18.
    PMID: 25273022 DOI: 10.1007/s00204-014-1376-6
    Carbon nanotubes (CNTs) are an important class of nanomaterials, which have numerous novel properties that make them useful in technology and industry. Generally, there are two types of CNTs: single-walled nanotubes (SWNTs) and multi-walled nanotubes. SWNTs, in particular, possess unique electrical, mechanical, and thermal properties, allowing for a wide range of applications in various fields, including the electronic, computer, aerospace, and biomedical industries. However, the use of SWNTs has come under scrutiny, not only due to their peculiar nanotoxicological profile, but also due to the forecasted increase in SWNT production in the near future. As such, the risk of human exposure is likely to be increased substantially. Yet, our understanding of the toxicological risk of SWNTs in human biology remains limited. This review seeks to examine representative data on the nanotoxicity of SWNTs by first considering how SWNTs are absorbed, distributed, accumulated and excreted in a biological system, and how SWNTs induce organ-specific toxicity in the body. The contradictory findings of numerous studies with regards to the potential hazards of SWNT exposure are discussed in this review. The possible mechanisms and molecular pathways associated with SWNT nanotoxicity in target organs and specific cell types are presented. We hope that this review will stimulate further research into the fundamental aspects of CNTs, especially the biological interactions which arise due to the unique intrinsic characteristics of CNTs.
    Matched MeSH terms: Environmental Exposure/adverse effects
  6. Zailina H, Junidah R, Josephine Y, Jamal HH
    Asia Pac J Public Health, 2008;20(4):317-26.
    PMID: 19124326 DOI: 10.1177/1010539508322697
    This study aimed to determine the relationship between blood lead (BPb) concentrations and cognitive and physical development in school children. A total of 169 urban children and 100 industrial children of Malay ethnicity, in the age range of 6(1/2) to 8(1/2) years, were selected. BPb was determined using GF atomic absorption spectrophotometer. The mean cognitive score (102.55) of the children from the industrial area was significantly higher than that of the urban children (95.09; P < .001). However, no significant differences were found in the BPb levels between the 2 groups (industrial, 3.75 microg/dL; urban, 3.56 microg/dL). There was significant inverse correlation between BPb and cognitive scores for all children (P < .05). The cognitive scores for all children were influenced by BPb after adjustments (P < .05). The urban children had significantly better Weight for Height and Left Arm Circumference values than those from industrial area. There was no significant correlation between BPb and the anthropometric measurements. In conclusion, low BPb influenced the cognitive development, whereas physical development was not affected.
    Matched MeSH terms: Environmental Exposure/adverse effects*
  7. 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
  8. 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
  9. Subahir MN, Shah SA, Zainuddin ZM
    Asian Pac J Cancer Prev, 2009;10(6):1015-20.
    PMID: 20192575
    INTRODUCTION: In Malaysia, prostate cancer is ranked 6th among male cancer and expected to increase in the future. Several factors have shown to be related to prostate cancer such as sociodemographic, lifestyle, diet, occupational exposure, medical and health status. This is the first time a similar study was conducted in Malaysia to recognize the risk factors for prostate cancer patients who came for treatment at University Kebangsaan Malaysia Medical Centre (UKMMC).

    METHODS: Prostate cancer cases diagnosed between 2003 and 2008 which met with the inclusion criteria were included in the study. One hundred and twelfth (112) pairs of cases and controls matched by age and ethnicity were analysed. McNemar Odds Ratios (OR(M)) were calculated using McNemar Calculator software for univariate analysis while conditional logistic regression was used for multivariate analysis, both using SPSS version 12.0.

    RESULTS: Most of the prostate cancer patients (68.8%) that came for treatment in UKMMC were above 70 years old. The majority were Chinese (50.0%) followed by Malay (46.4%) and Indian (3.6%). Multivariate analysis showed cases were more likely to have a first-degree relative with a history of cancer (OR= 3.77, 95% CI= 1.19-11.85), to have been exposed to pesticides (OR= 5.57, 95% CI= 1.75-17.78) and consumed more meat (OR= 12.23, 95% CI= 3.89-39.01). Significantly reduced risks of prostate cancer were noted among those consuming more vegetables (OR= 0.12, 95% CI= 0.02-0.84), more tomatoes (OR= 0.35, 95% CI= 0.13-0.93) and those who had frequent sexual intercourse (OR= 0.44, 95% CI= 0.19-0.96).

    CONCLUSION: Some lifestyle and occupation factors are strong predictors of the occurrence of prostate cancer among patients in UKMMC. More importantly, with the identification of the potentially modifiable risk factors, proper public health intervention can be improved.

    Matched MeSH terms: Environmental Exposure/adverse effects
  10. 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
  11. 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*
  12. 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
  13. Magalingam KB, Radhakrishnan A, Ping NS, Haleagrahara N
    Biomed Res Int, 2018;2018:3740461.
    PMID: 29707568 DOI: 10.1155/2018/3740461
    Neurodegenerative diseases are hereditary or sporadic conditions that result in the progressive loss of the structure and function of neurons as well as neuronal death. Although a range of diseases lie under this umbrella term, Alzheimer's disease (AD) and Parkinson's disease (PD) are the most common neurodegenerative diseases that affect a large population around the globe. Alzheimer's disease is characterized by the abnormal accumulation of extracellular amyloid-β plaques and intraneuronal neurofibrillary tangles in brain regions and manifests as a type of dementia in aged individuals that results in memory loss, multiple cognitive abnormalities, and intellectual disabilities that interfere with quality of life. Since the discovery of AD, a wealth of new information has emerged that delineates the causes, mechanisms of disease, and potential therapeutic agents, but an effective remedy to cure the diseases has not been identified yet. This could be because of the complexity of the disease process, as it involves various contributing factors that include environmental factors and genetic predispositions. This review summarizes the current understanding on neurodegenerative mechanisms that lead to the emergence of the pathology of AD.
    Matched MeSH terms: Environmental Exposure/adverse effects
  14. 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*
  15. 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*
  16. Narayanan KB, Ali M, Barclay BJ, Cheng QS, D'Abronzo L, Dornetshuber-Fleiss R, et al.
    Carcinogenesis, 2015 Jun;36 Suppl 1:S89-110.
    PMID: 26106145 DOI: 10.1093/carcin/bgv032
    Cell death is a process of dying within biological cells that are ceasing to function. This process is essential in regulating organism development, tissue homeostasis, and to eliminate cells in the body that are irreparably damaged. In general, dysfunction in normal cellular death is tightly linked to cancer progression. Specifically, the up-regulation of pro-survival factors, including oncogenic factors and antiapoptotic signaling pathways, and the down-regulation of pro-apoptotic factors, including tumor suppressive factors, confers resistance to cell death in tumor cells, which supports the emergence of a fully immortalized cellular phenotype. This review considers the potential relevance of ubiquitous environmental chemical exposures that have been shown to disrupt key pathways and mechanisms associated with this sort of dysfunction. Specifically, bisphenol A, chlorothalonil, dibutyl phthalate, dichlorvos, lindane, linuron, methoxychlor and oxyfluorfen are discussed as prototypical chemical disruptors; as their effects relate to resistance to cell death, as constituents within environmental mixtures and as potential contributors to environmental carcinogenesis.
    Matched MeSH terms: Environmental Exposure/adverse effects*
  17. Langie SA, Koppen G, Desaulniers D, Al-Mulla F, Al-Temaimi R, Amedei A, et al.
    Carcinogenesis, 2015 Jun;36 Suppl 1:S61-88.
    PMID: 26106144 DOI: 10.1093/carcin/bgv031
    Genome instability is a prerequisite for the development of cancer. It occurs when genome maintenance systems fail to safeguard the genome's integrity, whether as a consequence of inherited defects or induced via exposure to environmental agents (chemicals, biological agents and radiation). Thus, genome instability can be defined as an enhanced tendency for the genome to acquire mutations; ranging from changes to the nucleotide sequence to chromosomal gain, rearrangements or loss. This review raises the hypothesis that in addition to known human carcinogens, exposure to low dose of other chemicals present in our modern society could contribute to carcinogenesis by indirectly affecting genome stability. The selected chemicals with their mechanisms of action proposed to indirectly contribute to genome instability are: heavy metals (DNA repair, epigenetic modification, DNA damage signaling, telomere length), acrylamide (DNA repair, chromosome segregation), bisphenol A (epigenetic modification, DNA damage signaling, mitochondrial function, chromosome segregation), benomyl (chromosome segregation), quinones (epigenetic modification) and nano-sized particles (epigenetic pathways, mitochondrial function, chromosome segregation, telomere length). The purpose of this review is to describe the crucial aspects of genome instability, to outline the ways in which environmental chemicals can affect this cancer hallmark and to identify candidate chemicals for further study. The overall aim is to make scientists aware of the increasing need to unravel the underlying mechanisms via which chemicals at low doses can induce genome instability and thus promote carcinogenesis.
    Matched MeSH terms: Environmental Exposure/adverse effects*
  18. Hu Z, Brooks SA, Dormoy V, Hsu CW, Hsu HY, Lin LT, et al.
    Carcinogenesis, 2015 Jun;36 Suppl 1:S184-202.
    PMID: 26106137 DOI: 10.1093/carcin/bgv036
    One of the important 'hallmarks' of cancer is angiogenesis, which is the process of formation of new blood vessels that are necessary for tumor expansion, invasion and metastasis. Under normal physiological conditions, angiogenesis is well balanced and controlled by endogenous proangiogenic factors and antiangiogenic factors. However, factors produced by cancer cells, cancer stem cells and other cell types in the tumor stroma can disrupt the balance so that the tumor microenvironment favors tumor angiogenesis. These factors include vascular endothelial growth factor, endothelial tissue factor and other membrane bound receptors that mediate multiple intracellular signaling pathways that contribute to tumor angiogenesis. Though environmental exposures to certain chemicals have been found to initiate and promote tumor development, the role of these exposures (particularly to low doses of multiple substances), is largely unknown in relation to tumor angiogenesis. This review summarizes the evidence of the role of environmental chemical bioactivity and exposure in tumor angiogenesis and carcinogenesis. We identify a number of ubiquitous (prototypical) chemicals with disruptive potential that may warrant further investigation given their selectivity for high-throughput screening assay targets associated with proangiogenic pathways. We also consider the cross-hallmark relationships of a number of important angiogenic pathway targets with other cancer hallmarks and we make recommendations for future research. Understanding of the role of low-dose exposure of chemicals with disruptive potential could help us refine our approach to cancer risk assessment, and may ultimately aid in preventing cancer by reducing or eliminating exposures to synergistic mixtures of chemicals with carcinogenic potential.
    Matched MeSH terms: Environmental Exposure/adverse effects*
  19. 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*
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