Arsenic projects in SE Asia

2016 ◽  
Vol 31 (1) ◽  
Author(s):  
Panida Navasumrit ◽  
Krittinee Chaisatra ◽  
Mathuros Ruchirawat

AbstractEarly life exposure to inorganic arsenic is associated with a wide range of malignant and chronic disease outcomes in humans. Prenatal arsenic exposure may give rise to adverse effects on child health and development as arsenic readily passes through the placenta in human beings. The impact of maternal arsenic exposure on fetal gene expression was conducted in pregnant women living in Southern Thailand. Arsenic exposed newborns had significantly higher levels of arsenic in cord blood, and a set of genes associated with numerous biological pathways, including cell signaling, apoptosis, inflammatory and stress response. A slight increase in promoter methylation of

2016 ◽  
Vol 7 (5) ◽  
pp. 433-439 ◽  
Author(s):  
S. L. Prescott ◽  
K. Allen ◽  
K. Armstrong ◽  
C. Collins ◽  
H. Dickinson ◽  
...  

The evidence underpinning the developmental origins of health and disease (DOHaD) is overwhelming. As the emphasis shifts more towards interventions and the translational strategies for disease prevention, it is important to capitalize on collaboration and knowledge sharing to maximize opportunities for discovery and replication. DOHaD meetings are facilitating this interaction. However, strategies to perpetuate focussed discussions and collaborations around and between conferences are more likely to facilitate the development of DOHaD research. For this reason, the DOHaD Society of Australia and New Zealand (DOHaD ANZ) has initiated themed Working Groups, which convened at the 2014–2015 conferences. This report introduces the DOHaD ANZ Working Groups and summarizes their plans and activities. One of the first Working Groups to form was the ActEarly birth cohort group, which is moving towards more translational goals. Reflecting growing emphasis on the impact of early life biodiversity – even before birth – we also have a Working Group titled Infection, inflammation and the microbiome. We have several Working Groups exploring other major non-cancerous disease outcomes over the lifespan, including Brain, behaviour and development and Obesity, cardiovascular and metabolic health. The Epigenetics and Animal Models Working Groups cut across all these areas and seeks to ensure interaction between researchers. Finally, we have a group focussed on ‘Translation, policy and communication’ which focusses on how we can best take the evidence we produce into the community to effect change. By coordinating and perpetuating DOHaD discussions in this way we aim to enhance DOHaD research in our region.


Water ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 612 ◽  
Author(s):  
Monia Renzi ◽  
Valentina H. Pauna ◽  
Francesca Provenza ◽  
Cristina Munari ◽  
Michele Mistri

Transitional water ecosystems (TWEs), despite their ecological and economic importance, are largely affected by human pressures that could be responsible for significant inputs of litter in the marine environment. Plastic input in coastal ponds, lagoons, river deltas and estuaries, could be driven by a wide range of human activities such as agriculture, waste disposal, municipal and industrial wastewater effluents, aquaculture, fishing and touristic activities and urban impacts. However, it remains unknown what the impact of plastic input in these TWEs could have on natural capital and, therefore, the ability for an ecosystem to provide goods and services to human beings. Given the large interest with regards to the conservation of transitional water ecosystems and the clear exposure risk to plastic and microplastic pollution, this study aims to perform: (i) a bibliometric analyses on existing literature regarding the levels of marine litter in such environments; (ii) a selection among the available literature of homogeneous data; and (iii) statistical analyses to explore data variability. Results suggest that: (i) research on microplastics in these ecosystems did not begin to be published until 2013 for lagoons, 2014 for river mouths and 2019 for coastal ponds. The majority of articles published on studies of microplastics in lagoons did not occur until 2019; (ii) sediments represent the matrix on which sampling and extraction variability allow the statistical analyses on data reported by the literature; (iii) the Analysis of Similarities (ANOSIM) test two-way evidenced that the level of protection of marine and terrestrial areas produced similar values while the habitat type showed low significance in terms of its effect on microplastic levels, shape and size in sediments.


2010 ◽  
Vol 103 (9) ◽  
pp. 1278-1286 ◽  
Author(s):  
Rachel L. Thompson ◽  
Lisa M. Miles ◽  
Joanne Lunn ◽  
Graham Devereux ◽  
Rebecca J. Dearman ◽  
...  

The aim of the present systematic review was to evaluate the influence of early life exposure (maternal and childhood) to peanuts and the subsequent development of sensitisation or allergy to peanuts during childhood. Studies were identified using electronic databases and bibliography searches. Studies that assessed the impact of non-avoidance compared with avoidance or reduced quantities of peanuts or peanut products on either sensitisation or allergy to peanuts, or both outcomes, were eligible. Six human studies were identified: two randomised controlled trials, two case–control studies and two cross-sectional studies. In addition, published animal and mechanistic studies, relevant to the question of whether early life exposure to peanuts affects the subsequent development of peanut sensitisation, were reviewed narratively. Overall, the evidence reviewed was heterogeneous, and was limited in quality, for example, through lack of adjustment for potentially confounding factors. The nature of the evidence has therefore hindered the development of definitive conclusions. The systematic review of human studies and narrative expert-led reviews of animal studies do not provide clear evidence to suggest that either maternal exposure, or early or delayed introduction of peanuts in the diets of children, has an impact upon subsequent development of sensitisation or allergy to peanuts. Results from some animal studies (and limited evidence from human subjects) suggest that the dose of peanuts is an important mediator of peanut sensitisation and tolerance; low doses tend to lead to sensitisation and higher doses tend to lead to tolerance.


2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Hongbo Men ◽  
Jamie L. Young ◽  
Wenqian Zhou ◽  
Haina Zhang ◽  
Xiang Wang ◽  
...  

Maternal exposure to cadmium causes obesity and metabolic changes in the offspring, including nonalcoholic fatty liver disease-like pathology. However, whether maternal cadmium exposure accelerates liver cancer in the offspring is unknown. This study investigated the impact of early-life exposure to cadmium on the incidence and potential mechanisms of hepatocellular carcinoma (HCC) in offspring subjected to postweaning HCC induction. HCC in C57BL/6J mice was induced by diethylnitrosamine (DEN) injection at weaning, followed by a long-term high-fat choline-deficient (HFCD) diet. Before weaning, liver cadmium levels were significantly higher in mice with early-life cadmium exposure than in those without cadmium exposure. However, by 26 and 29 weeks of age, hepatic cadmium fell to control levels, while a significant decrease was observed in copper and iron in the liver. Both male and female cadmium-exposed mice showed increased body weight compared to non-cadmium-treated mice. For females, early-life cadmium exposure also worsened insulin intolerance but did not significantly promote DEN/HFCD diet-induced liver tumors. In contrast, in male mice, early-life cadmium exposure enhanced liver cancer induction by DEN/HFCD with high incidence and larger liver tumors. The liver peritumor tissue of early-life cadmium-exposed mice exhibited greater inflammation and disruption of fatty acid metabolism, accompanied by higher malondialdehyde and lower esterified triglyceride levels compared to mice without cadmium exposure. These findings suggest that early-life exposure to low-dose cadmium accelerates liver cancer development induced by a DEN/HFCD in male mice, probably due to chronic lipotoxicity and inflammation caused by increased uptake but decreased consumption of fatty acids.


2019 ◽  
Vol 18 (2) ◽  
pp. 77-95
Author(s):  
Rashesh Shrestha

In this paper, I study the impact of early life exposure to air pollution caused by the 1997 Indonesian forest fires on cognitive ability, an important determinant of success in the labor market. To isolate the effect of pollution exposure, I use a difference-in-differences approach where exposure to pollution is determined by timing and region of birth. The results suggest that pollution lowered cognitive test score at age 8–9 years by 6 percent. I also estimate how this might translate into lost earnings on a different but comparable sample. The estimates suggest that natural disasters can reduce earnings by 5 to 8 percent by hampering cognitive ability. Lost earnings due to interrupted cognitive development could be an additional cost of exposure to air pollution.


2013 ◽  
Vol 280 (1772) ◽  
pp. 20131502 ◽  
Author(s):  
Jason R. Rohr ◽  
Thomas R. Raffel ◽  
Neal T. Halstead ◽  
Taegan A. McMahon ◽  
Steve A. Johnson ◽  
...  

Exposure to stressors at formative stages in the development of wildlife and humans can have enduring effects on health. Understanding which, when and how stressors cause enduring health effects is crucial because these stressors might then be avoided or mitigated during formative stages to prevent lasting increases in disease susceptibility. Nevertheless, the impact of early-life exposure to stressors on the ability of hosts to resist and tolerate infections has yet to be thoroughly investigated. Here, we show that early-life, 6-day exposure to the herbicide atrazine (mean ± s.e.: 65.9±3.48 µg l −1 ) increased frog mortality 46 days after atrazine exposure (post-metamorphosis), but only when frogs were challenged with a chytrid fungus implicated in global amphibian declines. Previous atrazine exposure did not affect resistance of infection (fungal load). Rather, early-life exposure to atrazine altered growth and development, which resulted in exposure to chytrid at more susceptible developmental stages and sizes, and reduced tolerance of infection, elevating mortality risk at an equivalent fungal burden to frogs unexposed to atrazine. Moreover, there was no evidence of recovery from atrazine exposure. Hence, reducing early-life exposure of amphibians to atrazine could reduce lasting increases in the risk of mortality from a disease associated with worldwide amphibian declines. More generally, these findings highlight that a better understanding of how stressors cause enduring effects on disease susceptibility could facilitate disease prevention in wildlife and humans, an approach that is often more cost-effective and efficient than reactive medicine.


Parasitology ◽  
1993 ◽  
Vol 106 (S1) ◽  
pp. S93-S107 ◽  
Author(s):  
D.R. Phillips

SUMMARYUrbanization involves a physical change in which increasing proportions of populations live in urban settings, however defined. It also implies considerable changes in the ways in which these people live, how they earn their livelihoods, the food which they eat, and the wide range of environmental factors to which they are exposed. There is another underlying assumption that, increasingly, urban populations will be more healthy than their rural counterparts and that higher levels of urbanization will equate with better health status. This paper discusses some of the assumptions underlying this contention. It takes issue with certain of them, particularly the assumption that urbanization affects the health of all residents equally. It is manifestly evident that in many cities, particularly in the developing world, the poor are exposed to greater risks and have much lower health status than their richer neighbours. In addition, whilst urban residents may theoretically have a better access to health care and services than do residents in many rural areas, and whilst many indicators of health do appear better in more highly urbanized societies than ones less so, there are caveats. The paper introduces the concept of epidemiological transition, which suggests that, whilst life expectancy might be higher in many urbanized countries and in certain cities, the inhabitants are often merely suffering from different forms of ill-health, often chronic or degenerative, rather than infective. In certain cities in middle-income countries, residents, particularly the poor, are exposed to a double risk of both infection and chronic degenerative ailments. The paper concludes with a consideration of more general recent statements from the World Health Organization among others, on the impact of urbanization on health. The ‘Healthy Cities’ project is also discussed. WHO identifies a range of general determinants of urban health: physical, social, cultural and environmental. Many represent the by-products of modernization and especially industrialization. It is emphasized that urbanization, and the concentration of human beings into new areas in particular, can bring exposure to new risk factors for large numbers of people. The growth of infectious and parasitic disease in some urban settings must therefore be recognized, as must the emergence of chronic diseases, with the concomitant need for investment in new types of health and social care. However, a number of constraints militate against the achievement of improved urban health, especially in developing countries. The paper concludes by considering some important constraints: the very scale of urban health problems; the impacts of structural adjustment programmes which cut public expenditure on environmental health, health services and nutrition, thereby increasing the vulnerability of the poor; urban management problems; lack of political will; and the difficulties of measuring change in health and effects of policies.


2009 ◽  
Vol 83 (6) ◽  
pp. 549-556 ◽  
Author(s):  
Shuhua Xi ◽  
Wenjuan Sun ◽  
Fengzhi Wang ◽  
Yaping Jin ◽  
Guifan Sun

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