Health Risk Assessment - Science topic

Hereby, I am delighted to offer a curated collection of scholarly articles from Environmental Science, carefully selected to enrich your research pursuits and foster further intellectual exploration.

1.Source Analysis and Health Risk Assessment of Heavy Metals in the Groundwater of Shijiazhuang, a Typical City in North China Plain

Article Link:https://jtp.oversea.cnki.net/Bilingual/detail/html/HJKZ202309011

2.Ambient VOCs Characteristics and Reactivity During O 3 Pollution in Autumn in Urban Beijing

Article Link:https://jtp.oversea.cnki.net/Bilingual/detail/html/HJKZ202302053

3.Deposition Characteristics of Water-soluble Inorganic Nitrogen and Organic Nitrogen in Atmospheric Precipitation in the Northern Suburbs of Nanjing

Article Link:https://jtp.oversea.cnki.net/Bilingual/detail/html/HJKZ202207005

4.Occurrence Characteristics of Microplastics and Metal Elements in the Surface Water of Huangpu River and Their Associations with Metal Resistance Genes

Article Link:https://jtp.oversea.cnki.net/Bilingual/detail/html/HJKZ202305014

5.Analysis of Change and Driving Factors of River Environmental Quality in China from 2002 to 2020

Article Link:https://jtp.oversea.cnki.net/Bilingual/detail/html/HJKZ202305010

"Health Risk" is usually measured as a concentration of a compound over time in a particular area. The toxicity levels of hazardous chemicals are catalogued by OSHA and the EPA. If you are looking for a dispersion model, the EPA used to have one that we used for Facility Risk Planning and Community organizations.

Hi Md. Shareful Hassan

some links:

Anyway, before applying I suggest to read carefully the manuals for pros & cons.

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.

What about COSHH? What about COSHH? it is focused not on the hazard but the risk for occupational health.

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.

Very good initiative. My best wishes!

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:

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.

Dear Abinaya Sekar,

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

S J Malik Thankyou

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.

Have a look at this useful RG link.

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

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.

According to the USEPA 2000, oral reference doses (mg/kg/day) for several metals are follows. Cr (III)=1.5 , Fe = 0.7, Cu = 0.04, Zn = 0.3, As = 0.014, Cd = 0.001, Pb = 0.004, Ni = 0.91

Drinking water be free from E coli.

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....

Check and read this usefull link...

https://ec.europa.eu/jrc/en/eurl/ecvam/alternative-methods-toxicity-testing/validated-test-methods/bioconcentration-and-bioaccumulation

All best

Hi Dear;

Please check them up:

Good Luck.

@Kajori Parial.....A colleague of mine has a day like that in Ghana. You can contact him on daikins@umat.edu.gh

Interesting

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.

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.

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?

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.

 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.

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

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

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

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

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.

hello

may be of interest

be well

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.

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.   

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.

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.

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. 

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.

The dynamic gait index would be a great tool. It tests walking, turning, single limb stance, functional reach, etc by Tinneti.

This may be of interest: The Impact on Health of Emissions to Air from Municipal Waste Incinerators RCE 13

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!

There is sometimes confusion between 'exposure' and 'absorption' when calculating chemical risks.  This paper is helpful:

Regards

Dale

Hi Parth,

You can see this papers,

Best regards,

This approach was applied in my research study in Czech republic:

You can download this paper: https://www.researchgate.net/publication/38082931_Soil_burdens_of_persistent_organic_pollutants--their_levels_fate_and_risks_Part_III._Quantification_of_the_soil_burdens_and_related_health_risks_in_the_Czech_Republic?ev=prf_pub

Best regards,

Pavel

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!!

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.

I am pleased to send you a document which explain the " Modulation by magnesium of N-methyl-D-aspartate receptors in developing human brain."

If need more please ask me by mail to me