Questions related to Health Risk Assessment
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.
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?
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?
In detailed human health risk assessment models. Is there any model that can predict the possible disease.
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?
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?
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?
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.
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.
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.
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?
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?
Risk assessment of human health due to acute and chronic exposure of atmospheric Polyaromatic Hydrocarbons (PAHs) using suitable biomarker in urban and rural area.
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.
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.
Ambient air pollution, Benzene (α) Pyrene, Biomarker, Carcinogenicity, Risk assessment
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
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.
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.
I'm working on cumulative risks assessment of lead, chronium, nickel in groundwater and drinking water.
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?
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.
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?
my research is on human health risk assessment of emission from jamshoro thermal power plants using gaussion plume model
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.
Human health risk assessment for water quality of rivers through trace element and heavy metals contact
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.
I'm trying to design a study aimed at assessing risk percpetion in a smaple of climbing and/or via ferrata practitioners.
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?
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?
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?
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
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?
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?
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 ?
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.
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.
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" .
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.
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.
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
Do you know any software which could be an alternative to the RBCA software toolkit for chemical releases to perform risk assessment evaluations?
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?
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).
To what extent is susceptibility and coping ability included in the current practice of doing HHRA? How is uncertainty addressed?