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or the possible source i might be able to acquire it from. I have already tried it to find it from USEPA but was unable to find it.
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Well, I guess one of the advantages(?) of redefining "standards" is all of the additional work it creates for researchers! The definitive EPA Paper on defining RfDs from other factors is in the following reference. Chlorides and chlorine toxicity data have been around for a long time, so you should be able to tweak them to the EPA's liking.
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“evaluation of health hazards and health risk assessment” What is the difference between them? What are their different steps?
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What about COSHH? What about COSHH? it is focused not on the hazard but the risk for occupational health.
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Human biomonitoring (HBM) is a tool of health-related environmental monitoring with which populations are examined for their exposure to pollutants from the environment. The results are also intended to provide information as to whether (further) pollutant reduction measures are needed and on the effects of existing measures. HBM plays an essential role in environmental health and the assessment of pollution levels in the population, population groups or individuals. HBM makes it possible to determine levels of contamination in individuals and, where applicable, some of the biological effects triggered by it. It is thus subdivided into human biological monitoring of exposure and biological effect monitoring.
Based on your opinion, what do you think about the importance of using HBM in human health related studies?
Regards,
Ata
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Human biomonitoring allows us to measure our exposure to chemicals by measuring either the substances themselves, their metabolites or markers of subsequent health effects in body fluids or tissues. Information on human exposure can then be linked to data on sources and epidemiological surveys, in order to inform research on the exposure-response relationships in humans.
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I am working on human health risk assessment from exposure to heavy metals in ground water through ingestion and dermal route. I am calculating separately for adults, children and infants because of the different ingestion rate.
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Very good initiative. My best wishes!
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Hi,
I need a description; of which formula to be used to calculate sample-wise human health risk assessment (HHRA) of non-carcinogenic groundwater contaminants? However, normally I have seen two kinds of formulas to be used one is an older version and another one is shortened or updated version. So, in that regard, I am a little bit confused; which formula should be suitable to calculate non-carcinogenic (HHRA) or is there any specific condition to use each of them?
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Potential non-carcinogenic risks for exposure to contaminants are assessed by comparison of the calculated contaminant exposures with respect to each exposure route and the reference dose (RfD) so as to produce the hazard quotient (HQ). The toxic risk due to potentially hazardous substances in the same environmental media is presumed to be additive and the arithmetic sum of individual target hazard quotient and is equal to the hazard index (HI). To estimate the overall potential for non-carcinogenic effects posed by potentially hazardous substances, the computed HQs for each element are integrated and expressed as a hazard index (HI). The metal pollution index is then, defined by HQ/HI. According to the USEPA (1989) where, HQ/HI < 1, there is no concern for potential human health risks caused by exposure to non-carcinogenic elements and where, HQ/HI >1, there may be a concern for potential human health risks caused by
exposure to non-carcinogenic elements.
You may refer to the publication below:
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If it could, is there any health risk if we consume the plants?
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Formalin (37% formaldehyde) would kill the root cells unless it is substantially diluted by water or other substances. Any absorption by the dead cells would then be by non-biological physico-chemical processes.
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In detailed human health risk assessment models. Is there any model that can predict the possible disease.
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You provided a sensational, innovative concept of predictive research based on the correlation between the level of air pollution (including the level of smog, emissions of toxic substances emitted from classic energy based on the combustion of fossil fuels and from motor vehicles powered by internal combustion engines) and the health of citizens living in specific areas, regions with a certain level of air pollution. In my opinion, if on the Internet, on specific websites and portals presenting these issues, including social media portals, there is an appropriate amount of data on this subject and official, reliably collected data are published and presented on the websites of public institutions and research centers dealing with the state of citizens' health and the state of air pollution, a research method based on sentiment analysis carried out on Big Data Analytics analytical platforms can be used, and the obtained data can be presented within the developed forms of reporting in Business Intelligence applications. In this way, you can develop a method of predictive analyzes tailored to the specificity of specific data sources.
Best wishes,
Happy New Year 2021
Dariusz Prokopowicz
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Controversial pre-publication results suggest SARS-CoV-2 RNAs may be reverse transcribed in human cells by reverse transcriptase (RT) from LINE-1 elements, integrated into the cell genome, and subsequently transcribed. Furthermore, the authors argue that endogenous LINE-1 expression can be induced upon SARS-CoV-2 infection or by cytokine exposure, suggesting a possible molecular mechanism for SARS-CoV-2 retro-integration in patients with Cov-2. These somewhat frightening preprint observations suggest potential long-term impacts from some Cov-2 infections (https://doi.org/10.1101/2020.12.12.422516). Are the authors doing a public service by releasing this preprint or might this negatively impact some public behavior on the vaccines?
However, now that these ideas are presented, they raise key questions as to how to efficiently test and assess integration and to adequately consider its potential long-term risk that would seem to merit wide spread scientific attention. How might we determine their clinical relevance and see if CoV-2 is rare or sufficiently frequent in infected individuals to be a public health concern? Are there efficient ways to refute or support the proposed integration and its mechanism? Would Southern blot experiments or genomic DNA sequencing with the integration site on multiple recovered patients be helpful and convincing?
In general, what types of experimental tests, data, and analyses are needed to convincingly test the ideas in this preprint and to determine whether or not SARS-CoV-2 is reverse-transcribed and integrated in the human genome. If this is occurring, then how can we best assess the frequency, and if there a resultant potential for chronic illness?
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S J Malik Thankyou
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In our country, a lot of water sources are found to be contaminated with arsenic (As). But, here, experts said that, using arsenic contaminated water is not harmful for us, we can use it in our daily needs except drinking.
My question is - using arsenic contaminated water for our daily needs, have any risk of bioaccumulation by surrounding biota? Does it have any associated human health risk?
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Drinking-water containg Arsenic increases the risks of cancer in the skin, lungs, bladder and kidney, as well as other skin changes such as hyperkeratosis and pigmentation changes.The effects on environments include death, inhibition of growth, photosynthesis and reproduction, and behavioral effects. Environments contaminated with arsenic contain only a few species and fewer numbers within species. If levels of arsenate are high enough, only resistant organisms, such as certain microbes, may be present. If arsenic poisoning occurs over a brief period of time, symptoms may include vomiting, abdominal pain, encephalopathy, and watery diarrhea that contains blood. Long-term exposure can result in thickening of the skin, darker skin, abdominal pain, diarrhea, heart disease, numbness, and cancer.
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Chromium is one of the main chemical ingredients of tannery industries. Those industries also produce a lot of chromium contaminated solid wastes. what are the biotransformation and bioaccumulation procedures it follows to expose in human body?
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Have a look at this useful RG link.
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Dear researchers your kind concern needed. I am working on groundwater pollution, however, I have to calculate the non-carcinogenic Human Health Risk Assessment of Nitrate and other parameters. In that regard, I need your valuable suggestion, and if anyone can send me a solved example file then I will be much thankful.
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NATURAL RESOURCES CORNELL COOPERATIVE EXTENSION
- Nitrate: Health Effects in Drinking Water
by
Margaret McCasland, Nancy M. Trautmann, and Keith S. Porter Center for Environmental Research
Nitrate is one of the most common groundwater contaminants in rural areas. It is regulated in drinking water primarily because excess levels can cause methemoglobinemia, or "blue baby" disease. Although nitrate levels that affect infants do not pose a direct threat to older children and adults, they do indicate the possible presence of other more serious residential or agricultural contaminants, such as bacteria or pesticides.
Nitrate in groundwater originates primarily from fertilizers, septic systems, and manure storage or spreading operations. Fertilizer nitrogen that is not taken up by plants, volatilized, or carried away by surface runoff leaches to the groundwater in the form of nitrate. This not only makes the nitrogen unavailable to crops, but also can elevate the concentration in groundwater above the levels acceptable for drinking water quality. Nitrogen from manure similarly can be lost from fields, barnyards, or storage locations. Septic systems also can elevate groundwater nitrate concentrations because they remove only half of the nitrogen in wastewater, leaving the remaining half to percolate to groundwater.
This bulletin focuses on the health effects of nitrate in drinking water, and another bulletin in this series (Fact sheet 400.04, Groundwater: What It Is and How to Protect It), addresses ways of protecting the quality of groundwater supplies.
What Is Nitrate?
Nitrate is an inorganic compound that occurs under a variety of conditions in the environment, both naturally and synthetically. Nitrate is composed of one atom of nitrogen (N) and three atoms of oxygen (O); the chemical symbol for nitrate is NO3. Nitrite (NO2) can be formed from nitrate by a chemical process called reduction. Nitrate does not normally cause health problems unless it is reduced to nitrite.
Nitrate in drinking water is measured either in terms of the amount of nitrogen present or in terms of both nitrogen and oxygen. The federal standard for nitrate in drinking water is 10 milligrams per liter (10 mg/l) nitrate-N, or 45 mg/l nitrate-NO3. when the oxygen is measured as well as the nitrogen. Unless otherwise specified, nitrate levels usually refer only to the amount of nitrogen present, and the usual standard, therefore, is 10 mg/l.
Short-term exposure to drinking water with a nitrate level at or just above the health standard of 10 mg/l nitrate-N is a potential health problem primarily for infants. Babies consume large quantities of water relative to their body weight, especially if water is used to mix powdered or concentrated formulas or juices. Also, their immature digestive systems are more likely than adult digestive tracts to allow the reduction of nitrate to nitrite. In particular, the presence of nitrite in the digestive tract of newborns can lead to a disease called methemoglobinemia.
Infant Feeding Practices to Minimize Intake of Nitrate and Nitrite
  1. Breast feeding. Little if any nitrate gets into breast milk, unless the mother is consuming very large quantities of nitrate. Also, bacterial contamination is not a problem when breast milk is consumed directly.
  2. Bottle feeding. Use already diluted liquid formulas or use low-nitrate water to dilute concentrated liquid or powdered formulas. Also, mixed formulas should be kept under refrigeration and used promptly to minimize bacterial reduction of nitrate to nitrite.
  3. Vegetables. Since many vegetables are high in nitrate, their consumption should be limited until an infant is 4-6 months old and their digestive tract has sufficiently matured. Your physician can help you decide when to add new foods. Vegetables should always be prepared while fresh and refrigerated promptly after cooking to minimize bacterial activity.
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I need to common method of evaluation of heavy metals content and human health risk assessment via consumption of vegetables, fruits and drinks from Selected Markets.
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Risk assessment procedures are based on source-pathway-receptor models and
involves the examination of site characteristics, environmental behavior and toxicity of the contaminant, its potential route of entry into the receptor (humans), exposure of the receptors to the contaminants and their response to the dose.
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It is suggested by USEPA 2009, used for health risk assessment studies in fish. For calculating the Hazard Index these oral RfD values will be used and I'm looking for this values of above-mentioned elements. 
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RfD for Cu= 0.04, Zn= 0.3, Mn= 0.14, Ni= 0.02, Cd= 0.001, Pb= 0.004, Cr= 1.5 Fe= 0.70 mg kg -1 day -1 (US EPA, 2000)
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Normally the national and international norms say: "No presence of E. coli UFC units, in a 100ml sample", but there is not difference between a sample with 10 UFC and other with 10,000?
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Drinking water be free from E coli.
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With abundant evidence in the literature that many health afflictions result from toxicant exposures, and with published NHANES data from CDC that most people have bioaccumulated numerous persistent toxicants within their body, why are medical students not taught about clinical toxicology and approaches to investigate and treat toxicant-related health problems?
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Project Title
Risk assessment of human health due to acute and chronic exposure of atmospheric Polyaromatic Hydrocarbons (PAHs) using suitable biomarker in urban and rural area.
Project Summary
Rationale of present study
Polyaromatic hydrocarbon (PAH) is currently a subject of extensive research. In recent decades, several studies around the world have shown a substantial exposure-response relationship with PAH due to its carcinogenic effects on human health. However, PAH and its associated derivatives with particles (PM10 and PM2.5) provide useful information about its diverse source, reactivity and carcinogenicity that have a significant increase in the mortality and morbidity rate. Therefore, it is necessary to study the carcinogenicity of PAH through the use of biomarkers and DNA adduct.
Scientific objectives
Taking these factors into account, the evaluation of PAH and its derivatives are very necessary from the point of view of health. The objective of this work was to estimate the PAH and its derivatives in PM10 and PM2.5.To identify potential sources of PAH and its derivatives via receptor model and its risk assessment.
Hypothesis to be tested
Polycyclic Aromatic Hydrocarbons (PAHs) are a major group of carcinogenic compounds mostly emitted from diesel exhaust (Autrup et al., 1999). Among PAH; highest level of Benzene (α) pyrene is found to be present in urban atmosphere and traces of Benzene (α) pyrene has been found to be present in human urine samples, especially from smokers and people occupationally exposed to PAHs (Jongeneelen et al., 1986). Benzene (α) pyrene, after
metabolic activation, forms adducts with cellular macromolecules, and these reaction products have been widely used to assess the exposure assessments of PAH. The 32P-postlabeling method has been used extensively to detect bulky carcinogen- DNA adducts in peripheral lymphocytes from occupationally exposed people and people living in areas with highest levels of PAH (Binkova et al., 1995; Parera et al., 1992).
Significance of this study
Due to insufficient information on the exposure of PAH on human health, it has been difficult to determine which PAH derivatives influences the morbidity and mortality rate. If health effects can be linked to PAH and its derivatives, such information would be very valuable in guiding control strategies. The total vehicular population of the Lucknow is 1,97,8345 as on 31.03.2017 which is 6.10% higher over the last year; however, petroleum sale has increased by 11.36% whereas sale of diesel has increased by 26.38% (IITR Lucknow report, 2017). Since diesel exhaust is the primary sources of PAH in ambient air of Lucknow, which has been used in huge ongoing construction activity (metro rail construction, roads, flyover construction, and multi-story apartment construction). Therefore, the risk assessment of PAH is necessary to know the severity of atmospheric PAH in urban area with the help of a suitable biomarker. The study is expected to provide the appropriate biomarker to identify the carcinogenicity associated with Polyaromatic Hydrocarbon.
Keywords
Ambient air pollution, Benzene (α) Pyrene, Biomarker, Carcinogenicity, Risk assessment
Objectives
1. To estimate the ambient air quality with respect to PM10 and PM2.5 at different locations (3) in urban area.
2. To determine the atmospheric PAH and its derivatives concentration in urban and rural environment.
3. To study the exposure characteristics of diesel, petrol and CNG vehicles.
4. To evaluate the potential risk of PAHs on subjects at rural and urban area.
5. To investigate the exposure of PAH and its derivatives by using Biomarker, PAH-albumin adduct, mitochondrial copy number, telomere length and genotoxicity using a competitive immunoassay.
6. To study the human health risk assessment and prioritization of PAH and its derivatives at rural and urban area.
Material and Methods
1. Overall Study Design
2. Monitoring of airborne pollutants (PM10, PM2.5, Gaseous Pollutants (SOx and NOx) Polyaromatic Hydrocarbon and Trace metals) based on methodology recommended by BIS and CPCB.
3. Exposure assessments of Diesel, Petrol and CNG in chamber.
4. Biological sampling for suitable biomarkers of PAH through Blood and Urine samples of subjects.
5. Immunoassay test for estimating carcinogenicity associated with PAH in human being
5.1.Isolation of Peripheral mononuclear white blood cells (PMBC) by standard Lymphored methods.
5.2. Quantification of B and T lymphocytes by (Simultest CD3/CD19, Becton-Dickinson, San Jose, CA).
5.3.32P-Postlabeling of DNA adducts by Nielsen et al., 1996 using the butanol enrichment procedure.
5.4. PAH- albumin adducts by using ELISA test (Autrup et al., 1995).
5.5.Determination of 1-hydroxypyrene by method used by (Hansen et al., 1993).
6. Risk assessment of PAH through suitable biomarker in studied area (USEPA 1990 method).
7. Receptor Modeling and Statistics.
Expected output and outcome of the proposal
It has been observed that several PAHs are probable or possible human carcinogens, most of which are known to be associated with atmospheric particles. Benzene (α) Pyrene (BaP), a plausible human carcinogen found to be present in ambient air, can be used as a biomarker of the carcinogenic risk of atmospheric PAH. Therefore, Benzene (α) Pyrene can be used in establishing air quality guideline when deriving a unit risk factor. Due to the widely varying physical and chemical properties of PAHs, their measurement is often difficult and expensive. The methodology for sampling, analysis and estimation of emissions should be harmonized to adequately assess current environmental concentrations, the effect of future control measures, and to refine any additional measures that may be required to adequately assess their impacts on human health. The influence of different types fuels burning (petrol, diesel and CNG) on ambient air quality status with respect to pollutants levels and established the emission factors of respective fuels. Identification of suitable biomarker due to higher levels of airborne pollutants
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Dear Dr. Your project is excellent and well planned. The most important thing is to analyze your data effeciently making correlation between level of atmospheric PAH and blood & urine levels of exposed persons. Also you mentioned trace elements in breif in M&M you should describe the relation between PAH and trace elements describing which type affected zn, selenium, cu, etc....
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As muscle is the main consumption part of the fishes, then what is the need to analyze the toxic elements in other tissues such as liver, gill and kidney?
Is that to check the accumulation pattern in different organs and their behavior? Or if you have any other suggestions, please give your comments.
Kind regards,
Anand.
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Dear all
Anybody knows how to participate into the WHO health statistics and health surveys which are published annually on the different healthcare topics and disorders? Of participation, I manily mean providing local data or modeling assessments.
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Hi !
Can anyone provide me any insight about availability of published/open access data of soil heavy metal/ trace element concentration with the GPS location? We are developing a model and need a good amount of spatial data to test the model.
However, it will be extremely helpful if any researcher/individual/ research group is having such data with them and is ready to share it with us for the above purpose. We will be citing the paper with due acknowledgement for the help extended.
For any further details please feel free to drop a message.
** N.B. : Data with concentrations above the permissible limit will be of much help.
Thanks in advance.
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@Kajori Parial.....A colleague of mine has a day like that in Ghana. You can contact him on daikins@umat.edu.gh
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I'm working on cumulative risks assessment of lead, chronium, nickel in groundwater and drinking water.
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Interesting
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I have found concentration of Arsenic and other metals less than LOQ of AAS. But, for the calculation of Hazard Quotient (HQ) do I need to calculate for the values that are less than LOQ?
Also, if I calculate the value it will be like (<2.30 or like this). Then for HI (which is the sum of individual HQ) how can I include that value in calculation?
Can you help me to get out of this situation?
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You have choices here. Less than the Limit of Quantification is not the same as zero, so assuming zero concentration would conflict with the principle of being conservative in health risk assessment. To be appropriately conservative, I recommend assuming that the concentration is half the distance between zero and the LOQ (0.5 x LOQ). Another possibility would be to use a different fraction, such as the fraction of samples in which the substance was detected; for example, if detected in 75 percent of samples, assume 0.75 x LOQ for all samples in which the substance was not detected.
I hope this helps. If you have further question, please feel free to contact me.
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We would like to either calculate CDI for different monthly periods after birth or for period of 1 year after birth for measured POPs concentrations in human milk. Would you recommend to use a traditional risk assessment approach for calculation of CDI, thus “CDI = C x IR x EF x ED / BW x AT” or would you alter the equation in some way? There are articles using just the following equation “CDI = C x IR / BW” however they do not take into account length of exposure and they produce significantly different results.
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Hello Anna. I read your question and wondered if the use of the traditional risk assessment approach is the best means of addressing the issue. It's not completely clear to me from your question what you would like to achieve by calculating the risks, but I would emphasise that using the risk assessment approach you mention will probably give you very conservative estimates of risk related to these chemical exposures. I would highly recommend that if you want to calculate realistic (i.e. non-conservative) estimates of risk, you should consider using epidemiological data to support your assessment i.e. calculate the attributable risk associated with exposure to these POPs using odds ratios (or relative risks) from epidemiological studies. Although the exposures and outcomes are different, I wrote a paper about how and why to use epidemiological data in support of risk assessment. I hope it's helpful.
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Nano-specific qualitative or semi-quantitative tools were developed for occupational exposure assessment. Some prominent examples are Stoffenmanager Nano and NanoSafer (Hristozov et al., Environment International 95 (2016) 36-53).
Are there any other modellig tool for a quantitative or semi-quantitative occupational exposure assessment to nanomaterials?
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Does someone know what is meant with "nanospesific" in exposure modeling? 
If it is just deposition, coagulation, and properties of particles the "nanospesific" models are developed long time ago (Nazaroff 1989; see ref above). Prof. Nazaroff used successfully multicompartment model to predict particle and gas concentration levels in a museum. He estimated soiling (deposition) of art pieces over long term exposure to outdoor concentration. This is an excellent example where we should aim at in exposure modelings; both particulate matter and gaseous pollutants should be taken into account and their mass flow to surfaces, human lungs, filters, outdoors should be solved.
Can someone explain why we started to use "semi-quantitative" and different "Tier level" modelings? We have made exposure modelings more complicated than it was during 80's. How this is possible?
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my research is on human health risk assessment of emission from jamshoro thermal power plants using gaussion plume model
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The HYSPLIT model is a complete system for manipulating simple air parcel trajectories to complex dispersion and deposition simulations. The model is a hybrid between the Lagrangian approach, which uses a moving frame of reference for the advection and diffusion calculations as the air parcels move from their initial location, and the Eulerian approach, which uses a fixed three-dimensional grid as a frame of reference to compute the pollutant air concentrations (Draxler 2007).The NOAA HYSPLIT model was used to apportion the source, direction of transportation and concentration of pollutants in the study areas. The model is a tool that helps explain how, when, and where potentially harmful materials are atmospherically transported, dispersed, and deposited.
To do all these, you must use gridded meteorological data(satellite acquired) of the study area to drive the trajectories and concentrations either forwards or backwards in time at regular time intervals.
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as we konwn,the caprini score is the tool for assessment the VTE risk ,especially for the patients undgoing surgery in the post-opertive period. and the model is maked by Pro caprini.
but ,i still donot understand the rantionale of the caprini score model, The first question , every risk factor has it's point,such as age 40-60 is 1point,age 60-74 represents 2 point, and so on, how to calculate the different point and what is the rationale, is there anyone can help me ,if you have some paper the intrdouce the method to creat the model? thanks a lot.
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 Thanks for Dumitru Casian,and i have send a email about this query to seek advice to the Pro caprini and i hope to receive some feedback.
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Human health risk assessment for water quality of rivers through trace element and heavy metals contact
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You can search into US EPA IRIS database for toxicological information about arsenic toxicity.
I'm sure that some quantitative data are reported for chronic oral reference dose, carcinogenicity and relative drinking water consumption.
The effects induced by the exposure is reported as endpoint.
I can suggest also the links from Dr Latshaw,  Dr Varga and Hakkinen
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 Human via cosmetics chemicals, deodorant, household products.    
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There are two ways for determining the human exposures to chemicals:
1) Exposure assessment. In this way, the levels of exposure to chemicals via different routes (inhalation, oral, dermal) will be determined. The exposure level is measured based on the frequency and duration of exposure as well as the concentration of chemical in interested media (air, water, cosmetics, and etc.,). In the case of exposure via air pollution, you may consult an industrial hygienist for further information.
2) Biological monitoring. In this way, the levels of the chemical itself, its metabolites or a suitable biochemical effect(s) will be determined in different matrices (blood, urine, saliva, and etc.). Measurements of bodily fluids or breath are considered better measurements of exposure than the values measured in the exposure media alone since they represent an individual’s actual absorbed dose.
To get a method for determination of chemical levels in human fluids, you should search the PubMed (http://www.ncbi.nlm.nih.gov/pubmed) and other databases such as Science direct (http://www.sciencedirect.com/) with suitable key words.
Hoping this will be helpful,
Esmaeel
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I am wondering if there are any computational methods to preform health risk assessment of workers exposed to ultrafine particles.Their size distribution and number dose in the lungs is known, but not their composition.
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It can be possible if the reference dose for PM in different parts of lung have been setup...MPPD is computational modal that is widely followed
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I'm trying to design a study aimed at assessing risk percpetion in a smaple of climbing and/or via ferrata practitioners.
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You might find the following paper useful:
Thomson, C. J., Morton, K. L., Carlson, S. R., & Rupert, J. L. (2012). The Contextual Sensation Seeking Questionnaire for skiing and snowboarding (CSSQ-S). Development of a sport specific scale. International Journal of Sport Psychology, 43(6), 503-521.
Best,
SB
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Please I need information on this topic
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Hi Ana-Maria,
Perhaps you may wish to consider single metrics (measuring an actual against an objective) individually, without summing them or performing other operations, for the sake of simplicity of presentation. The link to the OSH indicators is a good one. In general, for managing, distance metrics may be more useful in the short run were everything is more or less fixed. In the US OSHA (the feds) have a lot of information that may be useful to you as well.
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I read in the literature that it can affect oxidative phosphorylation and ATP synthesis in mitochondrion. I would like to know more details and more precision about how it affects them?
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Just out of curiosity, does anyone here have any ideas as to how contractors actually account for injuries and accidents when they are bidding for projects? It sounds a bit odd to me to make allowances for such events like "should one of my workers fall off the roof or shoot himself in the leg with a nail gun" in their estimates, doesn't it?
However, claims from work related injuries can be very expensive and damaging in many other ways. Contractors surely must make allowance for this somehow. But how? Any ideas?
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Interesting question Dominic. In addition to having insurance cover, I believe a good number of contractors in UK (especially) medium to large ones take a proactive approach by investing into measures (e.g. safety management systems, behavioral based safety, etc.) to prevent injuries and accidents from occurring. This is simply because it is far better to prevent than to 'cure' as for instance the reputational damage injuries and accidents can cause can be very dire to the extent that a contractor may struggle to win work. Therefore rather than costing to cover for accident occurrence, the issue really is costing to cover for investment into H&S to prevent accidents, and certainly the cost is passed to the client in the form of head office overheads or project-specific overheads. You may be interested in the work by Dr Elias Ikpe  on cost-benefit analysis of accident prevention on construction projects (http://wlv.openrepository.com/wlv/bitstream/2436/98842/1/Ikpe_PhD%2520thesis.pdf). I hope this helps.
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I'm interested to learn if anybody knows if there are any other risk assessment tools that assess history as well as present risk of abuse in frontline services i.e refuges, statutory agencies and support services? 
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SARA or ODARA or URICADV - sorry I haven't time to get references at the moment - you may find online
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Does anyone know of some related text on how and when was smoking "pack-years" established for the first time and anything on the validity of this exposure assessment method/tool? I
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Hello,
It might be this one (but I don't have the actual study): Kahn, HA. (1966) The Dorn study of smoking and mortality among U.S. veterans. Report on eight and one-half years of observation. Natl. Cancer
Inst. Monogr. 19; which was discussed in the document at the following link:
If it is not helpful or a better answer is not forthcoming from someone else, it may be necessary to do this old school by ordering some of the earlier publications cited in the reference lists of the papers you do have and then reviewing the reference lists in those earlier papers and so on.   
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IARC recently upgraded the classification of glyphosate to 2A.  In the following article in Nature, it is noted that IARC rejected studies of glyphosate submitted by industry.  It is not stated if the industry studies were conducted by CROs.
However, the more interesting question, is, if industry funded studies (whether for new pesticides, food additives or drugs) are not considered reliable, then, if not industry, who should be expected to conduct and pay for these studies to support new products?  
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I do not judge conflict of interest or legal framework, I only point out the scientific issues. Robust experimental designs and well conducted experiments are the only important issues. It doesn't matter who sponsor them.
Anyway, it is well known the publishing bias towards positive studies.
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I dont have the raw data of a research, only have the RR and its CI. Any way to calculate the ARR with only this information?
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I presume you mean by ARR the population attributable risk (PAR)(or % cases prevented if exposure zero)
to calculate this you need both RR and proportion of population exposed. (Pe)
PAR (%) = 100 x Pe(RR-1) / (Pe(RR-1) + 1)
Applying CIs for RRs would give a range of estimates.
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In Preclinical Risk Assessment the term "Adversity" is very important for the fate of a newly detected or developed compound. The level of exposure where an adverse effect is detected can limit the therapeutic window for the intended human clinical use.  
Should the term adverse only be used when a translatability to humans can not be ruled out ?
In consequence should it be only used for cross-species findings ?
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Adversity in medicine reminds me of the word "singularity" in Physics. For me ,it is a euphemism to describe something we cannot control or simply we do not know. 
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How can I use these quotients in arsenic exposure assessment through drinking water?
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Personally, I think they are the same concept.  There are caculated as ratio of the exposure estimate over an acceptable effect level, which used for lower tiered risk assessment. 
In addition, you can learn more methods of risk assessment methods in the follow reference.
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i am interested in finding or developing a fall risk assessment tool that looks specifically at a population of persons in an in-patient drug/ETOH facility. While I know that there is some overlap with other assessment tools, most of these assume acute or long-term care with a primarily older adult population and do not specifically address this population.
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The dynamic gait index would be a great tool. It tests walking, turning, single limb stance, functional reach, etc by Tinneti.
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Thermal treatments, like incineration, are consolidated methods to treat waste to recover thermal and electrical energy. Flue gas treatment technologies, if well operated, can permit to control pollution.
Public opinion and politicians sometimes claim that incineration plants or similar sites create serious problems to people's health, without citing scientific basis.
I would like to know if there are recent studies, from all over the world, about this topic, that can describe what happened when the site was monitored and exposure risk was calculated, or references to full scale studies (national level). I add a very interesting article which treated a specific case in Italy.
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This may be of interest: The Impact on Health of Emissions to Air from Municipal Waste Incinerators RCE 13
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To be used at 0, 3 and 6 monthly intervals.
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It depends on the population you are studying (e.g. adults vs adolescents etc). I would suggest checking out the CAPS website (University of California, San Francisco) - they have a lot of survey instruments for HIV researchers, prevention planners etc - as long as you cite CAPS as your source. 
Hope this helps!
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One of nonconformities of company in OHSAS 18001 was about risk assessment, as we did not use "exposure" in our analysis. I am seeking a method which considers "exposure" .
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There is sometimes confusion between 'exposure' and 'absorption' when calculating chemical risks.  This paper is helpful:
Regards
Dale
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I want to do a health risk assessment modelling study using measured values of particulate matter. Can anyone please suggest a windows based model that I can run and estimate health risk.
Thank you
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Breast Cancer has been the most frequently diagnosed cancer and the leading cause of cancer death worldwide. In Ghana it is the leading cause of cancer death which is very frustrating, what we are looking for now is whether the impact of family and reproductive poses a higher risk in the development of this disease.
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I am conducting a research on public parks for PAHs, PCBs, etc. I will then do risk analysis on about 16 individual PAHs and some indicator PCBs. The literature gives me some approaches, even though data on individual PAHs are scanty. I will therefore appreciate, if i could get some links into such risk calculations from soil analysis
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Do you know any software which could be an alternative to the RBCA software toolkit for chemical releases to perform risk assessment evaluations?
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I really appreciate your answer. There is a lack of this kind of regulaton in Spain and I have to face an important matter now that may have to be faced using RB techniques.
Thank you very much!!
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I am dealing with a problem about which I found no available literature: the comparison between results from observational epidemiological studies (e.g. excess risk of a pathology in a contaminated area) and modelled risk estimated through chemical fate-transport and dose-response toxicological models (e.g. excess lifetime cancer risk = 10^-5).
Suppose we have a model that predicts a certain excess cancer risk around an industrial plant and we have data from an observational cohort study on residents in the area. How to compare them?
I think it is generally not recommendable to directly compare risk models and observed data, at least until exposure duration, intensity, toxicological pathways, health endpoint considered etc. are really comparable.
Does anyone know any publication about this issue?
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Because of the uncertainty inherent in the current practice of risk assessment (NAS and U.S. EPA paradigm), and the limited nature of epidemiological studies (limited in the number of people sampled/responding), it is often the case that the two are not directly comparable. For example, risk assessment may identify an unacceptable cancer risk in an exposed population after a hypothetical chemical release. Such risk assessments typically use default/generic exposure parameters and U.S. EPA defined toxicity values, which may include an aggregate of uncertainty factors that range from 10 to 1,000,000. The result of risk characterization might be a cancer risk of 5E-05 (5 times the acceptable target risk of one-in-a-million or 1E-05). In contrast, a large epidemiological study of the hypothetically exposed population is unlikely to sample (get meaningful responses from) more than 10,000 persons, and consequently does not have sufficient power to validate the result of the risk characterization. In such cases, the risk characterization should be considered a tool for evaluating the potential health risk to the population with a clear understanding of the uncertainty inherent in its calculation. Where epidemiology can demonstrate an increase in the observed frequency of disease or effect AND risk assessment demonstrates increased risk of that disease or effect, is suggestive of a causal linkage.
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I work on health hazards related to water hardness essentially those related to high concentration of calcium with low magnesium concentration. According to the literature, experimental work suggests possible magnesium’s interference with some receptors particularly sensitive receptor N-methyl-D-aspartate. This receptor is active by some amino acids such as aspartate and glutamate which causing stimulation brain function such as learning and memory. Literature has reported that variation in extracellular ionic magnesium concentration from 0.1 to 0.4 mmol significantly reduce the response of central NMDA receptors (Berthelot, 2004).
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I am pleased to send you a document which explain the " Modulation by magnesium of N-methyl-D-aspartate receptors in developing human brain."
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To what extent is susceptibility and coping ability included in the current practice of doing HHRA? How is uncertainty addressed?
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If need more please ask me by mail to me