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Bisphenol A and its effects on the systemic organs of children

Zulkifli S, Rahman AA, Kadir SHSA, Nor NSM

Eur J Pediatr, 2021 Oct;180(10):3111-3127.
PMID: 33893858 DOI: 10.1007/s00431-021-04085-0

For the past two decades, growing research has been pointing to multiple repercussions of bisphenol A (BPA) exposure to human health. BPA is a synthetic oestrogen which primarily targets the endocrine system; however, the compound also disturbs other systemic organ functions, in which the magnitude of impacts in those other systems is as comparable to those in the endocrine system. To date, the discoveries on the association between BPA and health outcomes mainly came from animal and in vitro studies, with limited human studies which emphasised on children's health. In this comprehensive review, we summarised studies on human, in vivo and in vitro models to understand the consequences of pre-, post- and perinatal BPA exposure on the perinatal, children and adult health, encompassing cardiovascular, neurodevelopmental, endocrine and reproductive effects.Conclusion: Evidence from in vitro and animal studies may provide further support and better understanding on the correlation between environmental BPA exposure and its detrimental effects in humans and child development, despite the difficulties to draw direct causal relations of BPA effects on the pathophysiology of the diseases/syndromes in children, due to differences in body system complexity between children and adults, as well as between animal and in vitro models and humans. What is known: • Very limited reviews are available on how BPA adversely affects children's health. • Previous papers mainly covered two systems in children. What is new: • Comprehensive review on the detrimental effects of BPA on children health outcomes, including expectations on adult health outcomes following perinatal BPA exposure, as well as covering a small part of BPA alternatives. • Essentially, BPA exposure during pregnancy has huge impacts on the foetus in which it may cause changes in foetal epigenetic programming, resulting in disease onsets during childhood as well as adulthood.

Matched MeSH terms: Environmental Exposure/adverse effects
Fulltext Public perception on human exposure risk: A case study on endocrine disrupting compounds in the environment

Wee SY, Aris AZ, Yusoff FM, Praveena SM

Ecotoxicol Environ Saf, 2024 Jan 15;270:115830.
PMID: 38141339 DOI: 10.1016/j.ecoenv.2023.115830

Humans are exposed to environmental risks owing to the broad usage of endocrine disrupting compounds (EDCs). However, the subjective evaluation of risk levels and characteristics, as well as the variation in risk processing, have not been thoroughly examined. The objective was to understand the public's perception of the risk associated with human exposure to environmental EDCs and identify any variations in risk perception. In this pioneering study conducted within the distinctive social and cultural context of Malaysia, a developing nation, a quantitative analysis approach was employed to assess the subjective evaluation of risk levels and characteristics among the public while developing a risk perception model. Data gathered from surveys and questionnaires were analyzed to gather information on the public's perception of environmental and health issues pertaining to pesticides, hormones, plastics, medicines, and cosmetics. The analysis revealed that the majority of the public assessed the level of human exposure to environmental risks based on experiential processing, which was influenced by cognitive and affective variables. Interestingly, a higher proportion of individuals in the community had a low risk perception of environmental EDCs, surpassing the overall risk perception by 19.3%. Furthermore, the public showed significant awareness of environmental and health issues related to pesticides, hormones, and plastics but had a lesser inclination to acknowledge the vulnerability of humans to risks associated with medicines and cosmetics. These findings suggest that the public is likely to be exposed to environmental EDCs based on their current perceived risks, and that sociopsychological factors play a significant role in shaping perceptions and judgments. This understanding can inform the development of targeted risk management strategies and interventions to mitigate the potential harm caused by environmental EDCs.

Matched MeSH terms: Environmental Exposure/adverse effects
Fulltext Projecting non-communicable diseases attributable to air pollution in the climate change era: a systematic review

Karim N, Hod R, Wahab MIA, Ahmad N

BMJ Open, 2024 May 07;14(5):e079826.
PMID: 38719294 DOI: 10.1136/bmjopen-2023-079826

OBJECTIVES: Climate change is a major global issue with significant consequences, including effects on air quality and human well-being. This review investigated the projection of non-communicable diseases (NCDs) attributable to air pollution under different climate change scenarios.
DESIGN: This systematic review was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020 flow checklist. A population-exposure-outcome framework was established. Population referred to the general global population of all ages, the exposure of interest was air pollution and its projection, and the outcome was the occurrence of NCDs attributable to air pollution and burden of disease (BoD) based on the health indices of mortality, morbidity, disability-adjusted life years, years of life lost and years lived with disability.
DATA SOURCES: The Web of Science, Ovid MEDLINE and EBSCOhost databases were searched for articles published from 2005 to 2023.
ELIGIBILITY CRITERIA FOR SELECTING STUDIES: The eligible articles were evaluated using the modified scale of a checklist for assessing the quality of ecological studies.
DATA EXTRACTION AND SYNTHESIS: Two reviewers searched, screened and selected the included studies independently using standardised methods. The risk of bias was assessed using the modified scale of a checklist for ecological studies. The results were summarised based on the projection of the BoD of NCDs attributable to air pollution.
RESULTS: This review included 11 studies from various countries. Most studies specifically investigated various air pollutants, specifically particulate matter <2.5 µm (PM2.5), nitrogen oxides and ozone. The studies used coupled-air quality and climate modelling approaches, and mainly projected health effects using the concentration-response function model. The NCDs attributable to air pollution included cardiovascular disease (CVD), respiratory disease, stroke, ischaemic heart disease, coronary heart disease and lower respiratory infections. Notably, the BoD of NCDs attributable to air pollution was projected to decrease in a scenario that promotes reduced air pollution, carbon emissions and land use and sustainable socioeconomics. Contrastingly, the BoD of NCDs was projected to increase in a scenario involving increasing population numbers, social deprivation and an ageing population.
CONCLUSION: The included studies widely reported increased premature mortality, CVD and respiratory disease attributable to PM2.5. Future NCD projection studies should consider emission and population changes in projecting the BoD of NCDs attributable to air pollution in the climate change era.
PROSPERO REGISTRATION NUMBER: CRD42023435288.

Matched MeSH terms: Environmental Exposure/adverse effects
Fulltext Recent Techniques in Determining the Effects of Climate Change on Depressive Patients: A Systematic Review

Ab Kader NI, Yusof UK, Khalid MNA, Nik Husain NR

J Environ Public Health, 2022;2022:1803401.
PMID: 35978588 DOI: 10.1155/2022/1803401

Climate change is amongst the most serious issues nowadays. Climate change has become a concern for the scientific community as it could affect human health. Researchers have found that climate change potentially impacts human mental health, especially among depressive patients. However, the relationship is still unclear and needs further investigation. The purpose of this systematic review is to systematically evaluate the evidence of the association between climate change effects on depressive patients, investigate the effects of environmental exposure related to climate change on mental health outcomes for depressive patients, analyze the current technique used to determine the relationship, and provide the guidance for future research. Articles were identified by searching specified keywords in six electronic databases (Google Scholar, PubMed, Scopus, Springer, ScienceDirect, and IEEE Digital Library) from 2012 until 2021. Initially, 1823 articles were assessed based on inclusion criteria. After being analyzed, only 15 studies fit the eligibility criteria. The result from included studies showed that there appears to be strong evidence of the association of environmental exposure related to climate change in depressive patients. Temperature and air pollution are consistently associated with increased hospital admission of depressive patients; age and gender became the most frequently considered vulnerability factors. However, the current evidence is limited, and the output finding between each study is still varied and does not achieve a reasonable and mature conclusion regarding the relationship between the variables. Therefore, more evidence is needed in this domain study. Some variables might have complex patterns, and hard to identify the relationship. Thus, technique used to analyze the relationship should be strengthened to identify the relevant relationship.

Matched MeSH terms: Environmental Exposure/adverse effects
Assessment of swimming associated health effects in marine bathing beach: an example from Morib beach (Malaysia)

Praveena SM, Pauzi NM, Hamdan M, Sham SM

Mar Pollut Bull, 2015 Mar 15;92(1-2):222-6.
PMID: 25597267 DOI: 10.1016/j.marpolbul.2015.01.003

A survey among beachgoers was conducted to determine the swimming associated health effects experienced and its relationship with beach water exposure behaviour in Morib beach. For beach water exposure behaviour, the highest frequency of visit among the respondents was once a year (41.9%). For ways of water exposure, whole body exposure including head was the highest (38.5%). For duration of water exposure, 30.8% respondents prefer to be in water for about 30 min with low possibilities of accidental ingestion of beach water. A total of 30.8% of beachgoers in Morib beach were reported of having dermal symptoms. Bivariate analysis showed only water activity, water contact and accidental ingestion of beach water showed significant association with swimming associated health effects experienced by swimmers. This study output showed that epidemiological study can be used to identify swimming associated health effects in beach water exposed to faecal contamination.

Matched MeSH terms: Environmental Exposure/adverse effects*
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
Tuning into the travel health risks of music tourism

Lu TS, Flaherty GT

J Travel Med, 2018 01 01;25(1).
PMID: 30346571 DOI: 10.1093/jtm/tay106
Matched MeSH terms: Environmental Exposure/adverse effects*
Fulltext Association of exposure to air pollutants and risk of mortality among people living with HIV: a systematic review

Padhi BK, Khatib MN, Ballal S, Bansal P, Bhopte K, Gaidhane AM, et al.

BMC Public Health, 2024 Nov 22;24(1):3251.
PMID: 39578775 DOI: 10.1186/s12889-024-20693-5

BACKGROUND: People living with HIV (PLWH) are more vulnerable to infectious and non-infectious comorbidities due to chronic inflammation and immune dysfunction. Air pollution is a major global health risk, contributing to millions of deaths annually, primarily from cardiovascular and respiratory diseases. However, the link between air pollution and mortality risk in PLWH is underexplored. This systematic review assesses the association between exposure to pollutants such as particulate matter (PM), nitrogen dioxide (NO2), sulfur dioxide (SO2), ozone (O3), and carbon monoxide (CO) and mortality risk in PLWH.
METHODS: A systematic search of PubMed, Web of Science, and Embase was conducted for studies published up to August 2024. Eligibility criteria included cohort, case-control, and cross-sectional studies assessing air pollution exposure and mortality in PLWH. Nested-Knowledge software was used for screening and data extraction. The Newcastle-Ottawa Scale was applied for quality assessment. A narrative approach and tabular summarization were used for data synthesis and presentation.
RESULTS: Nine studies, mostly from China, demonstrated a significant association between long-term exposure to PM1, PM2.5, and PM10 and increased risks of AIDS-related and all-cause mortality in PLWH. Hazard ratios for mortality increased by 2.38-5.13% per unit increase in PM concentrations, with older adults (> 60), females, and those with lower CD4 counts (

Matched MeSH terms: Environmental Exposure/adverse effects
Exploring cancer development in adulthood: cholinesterase depression and genotoxic effect from chronic exposure to organophosphate pesticides among rural farm children

How V, Hashim Z, Ismail P, Md Said S, Omar D, Bahri Mohd Tamrin S

J Agromedicine, 2014;19(1):35-43.
PMID: 24417530 DOI: 10.1080/1059924X.2013.866917

Children are the vulnerable group in the agricultural community due to their early exposure to pesticides through the dynamic interplay between genetic predisposition, environment, and host-related factors. This study aims to identify the possible association between the depression in blood cholinesterase level and genotoxic effect among farm children. The results of micronuclei assay and comet assay showed that the reduced blood cholinesterase level from organophosphate pesticide exposure is significantly associated with an increase in chromosome breakage and DNA strand breaks. These genotoxicity end points suggest that farm children's cells experience early DNA damage that may lead to uncontrolled cell proliferation during their adulthood. Thus, farm children who grow up near pesticide-treated farmland have a higher probability of developing cancer than children with minimal or zero exposure to pesticides.

Matched MeSH terms: Environmental Exposure/adverse effects*
Fulltext The use of quantile regression to forecast higher than expected respiratory deaths in a daily time series: a study of New York City data 1987-2000

Soyiri IN, Reidpath DD

PLoS One, 2013;8(10):e78215.
PMID: 24147122 DOI: 10.1371/journal.pone.0078215

Forecasting higher than expected numbers of health events provides potentially valuable insights in its own right, and may contribute to health services management and syndromic surveillance. This study investigates the use of quantile regression to predict higher than expected respiratory deaths. Data taken from 70,830 deaths occurring in New York were used. Temporal, weather and air quality measures were fitted using quantile regression at the 90th-percentile with half the data (in-sample). Four QR models were fitted: an unconditional model predicting the 90th-percentile of deaths (Model 1), a seasonal/temporal (Model 2), a seasonal, temporal plus lags of weather and air quality (Model 3), and a seasonal, temporal model with 7-day moving averages of weather and air quality. Models were cross-validated with the out of sample data. Performance was measured as proportionate reduction in weighted sum of absolute deviations by a conditional, over unconditional models; i.e., the coefficient of determination (R1). The coefficient of determination showed an improvement over the unconditional model between 0.16 and 0.19. The greatest improvement in predictive and forecasting accuracy of daily mortality was associated with the inclusion of seasonal and temporal predictors (Model 2). No gains were made in the predictive models with the addition of weather and air quality predictors (Models 3 and 4). However, forecasting models that included weather and air quality predictors performed slightly better than the seasonal and temporal model alone (i.e., Model 3 > Model 4 > Model 2) This study provided a new approach to predict higher than expected numbers of respiratory related-deaths. The approach, while promising, has limitations and should be treated at this stage as a proof of concept.

Matched MeSH terms: Environmental Exposure/adverse effects
Urban vs. rural factors that affect adult asthma

Jie Y, Isa ZM, Jie X, Ju ZL, Ismail NH

Rev Environ Contam Toxicol, 2013;226:33-63.
PMID: 23625129 DOI: 10.1007/978-1-4614-6898-1_2

In this review, our aim was to examine the influence of geographic variations on asthma prevalence and morbidity among adults, which is important for improving our understanding, identifying the burden, and for developing and implementing interventions aimed at reducing asthma morbidity. Asthma is a complex inflammatory disease of multifactorial origin, and is influenced by both environmental and genetic factors. The disparities in asthma prevalence and morbidity among the world's geographic locations are more likely to be associated with environmental exposures than genetic differences. In writing this article, we found that the indoor factors most consistently associated with asthma and asthma-related symptoms in adults included fuel combustion, mold growth, and environmental tobacco smoke in both urban and rural areas. Asthma and asthma-related symptoms occurred more frequently in urban than in rural areas, and that difference correlated with environmental risk exposures, SES, and healthcare access. Environmental risk factors to which urban adults were more frequently exposed than rural adults were dust mites,high levels of vehicle emissions, and a westernized lifestyle.Exposure to indoor biological contaminants in the urban environment is common.The main risk factors for developing asthma in urban areas are atopy and allergy to house dust mites, followed by allergens from animal dander. House dust mite exposure may potentially explain differences in diagnosis of asthma prevalence and morbidity among adults in urban vs. rural areas. In addition, the prevalence of asthma morbidity increases with urbanization. High levels of vehicle emissions,Western lifestyles and degree of urbanization itself, may affect outdoor and thereby indoor air quality. In urban areas, biomass fuels have been widely replaced by cleaner energy sources at home, such as gas and electricity, but in most developing countries, coal is still a major source of fuel for cooking and heating, particularly in winter. Moreover, exposure to ETS is common at home or at work in urban areas.There is evidence that asthma prevalence and morbidity is less common in rural than in urban areas. The possible reasons are that rural residents are exposed early in life to stables and to farm milk production, and such exposures are protective against developing asthma morbidity. Even so, asthma morbidity is disproportionately high among poor inner-city residents and in rural populations. A higher proportion of adult residents of nonmetropolitan areas were characterized as follows:aged 55 years or older, no previous college admission, low household income, no health insurance coverage, and could not see a doctor due to healthcare service availability, etc. In rural areas, biomass fuels meet more than 70% of the rural energy needs. Progress in adopting modern energy sources in rural areas has been slow. The most direct health impact comes from household energy use among the poor, who depend almost entirely on burning biomass fuels in simple cooking devices that are placed in inadequately ventilated spaces. Prospective studies are needed to assess the long-term effects of biomass smoke on lung health among adults in rural areas.Geographic differences in asthma susceptibility exist around the world. The reason for the differences in asthma prevalence in rural and urban areas may be due to the fact that populations have different lifestyles and cultures, as well as different environmental exposures and different genetic backgrounds. Identifying geographic disparities in asthma hospitalizations is critical to implementing prevention strategies,reducing morbidity, and improving healthcare financing for clinical asthma treatment. Although evidence shows that differences in the prevalence of asthma do exist between urban and rural dwellers in many parts of the world, including in developed countries, data are inadequate to evaluate the extent to which different pollutant exposures contribute to asthma morbidity and severity of asthma between urban and rural areas.

Matched MeSH terms: Environmental Exposure/adverse effects
The influence of low blood lead concentrations on the cognitive and physical development of primary school children in Malaysia

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*
Fulltext Clearing the air about "the haze"

Jeyaindran S

Med J Malaysia, 2006 Mar;61(1):117-21.
PMID: 16708750

From the beginning of time, man has lived in a continuous state of interdependence with his environment. If the forces of nature are harnessed well, they are a source of great benefit to mankind, but when this balance is tipped, nature's backlash on man can be quite devastating. In recent times, we have seen many vivid examples of the magnitude of the destructive forces of nature, ranging from massive floods caused by typhoons such as Katrina and Rita, the hundreds of thousands of lives lost by the powerful tsunami and the destruction of the environment by the raging forest fires in Spain and California. Yet man has not learnt his lesson. Often greed, at times gross ignorance and more often than not, just indifference to the effects of his actions on the environment result in man upsetting his balance with the environment. In Malaysia, since 1990, the haze has become a predictable annual occurrence, varying only in its severity and duration. The cause being beyond our control, we are unable to prevent it from happening. However, it is within our means to be ready to take the necessary steps to minimize the effects of the haze on the health of Malaysians. In order to be able to give appropriate advice and to allay the anxiety of the general public, it is necessary to have a clear understanding about the various effects of haze on humans.

Matched MeSH terms: Environmental Exposure/adverse effects*
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
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*
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
Fulltext Disruptive environmental chemicals and cellular mechanisms that confer resistance to cell death

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*
Fulltext Causes of genome instability: the effect of low dose chemical exposures in modern society

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*
Fulltext Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: focus on the cancer hallmark of tumor angiogenesis

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*
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*

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