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Toxicology Examination of a Site Research Paper

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Updated: May 27th, 2020

Site Overview

The derelict site was hitherto used by two industries, which have remained nonfunctional for the past sixty years. There are 100 drums buried underground and, unfortunately, their contents are not indicated. The drums show a sign of cracking and a, strong pungent, smell is felt in the air at the site. This must be a clear indication that they contain Toluene diisocyanate (TDI) and other unsafe chemicals.

The two companies are known for producing wastes rich in Polychlorinated biphenyls (PCBs), which are dangerous organic compounds. PCBs are banned by Stockholm Convention because they are persistent organic pollutants (Lu & Kacew, 2009). Other wastes generated by the company include chromium, Toluene diisocyanate (TDI) and Acryl amide.

All these compounds have adverse effects on human health and the general environment. Fishing activities takes place in a stream which flows through the polluted and contaminated site.

There is a residential area about a mile downstream of the site and the residents draw their domestic water from that place. The same water from the stream is used for irrigation downstream, which is a serious health hazard to the crops, and consequently human health.

Waste Analysis

The following is an analysis of the polluted site with PCBs, chromium wastes, Acrylamide and TDI. It describes the four contaminants covering their routes of exposure, mechanisms of toxicity and the permissible limits of exposure. The report is to assist in risk assessment and management (Larry & Hansen, 2001).

Polychlorinated Biphenyls (PCBs)

Polychlorinated biphenyl is an organo-chloride substance used in industries for production of several products. It was banned due to its persistent effect on living organisms and their environment. Exposure routes for PCBs are enormous including fish consumption of contaminated fish especially from Fox River and Lake Michigan. Ducks and other animals which feed from polluted sources are also exposure channels.

Inhalation of polluted air is a significant route of exposure as well as dermal route when PCBs dust settle on cars and other objects (Larry & Hansen, 2001). Drinking water from polluted water sources also exposes people to this toxicant because PCBs settle on water and can, therefore, be taken into the body during drinking. Infants in the womb, as well as during breast feeding, are exposed to their motherโ€™s PCBs.

PCBs have several mechanisms of toxicity. Introduction of PCBs suppress the body immune system thus predisposing one to many diseases. Major mechanisms include both independent and dependent Ah receptor mechanisms which result in endocrine disruption. Exposures lead to the formation of ortho-substituted congeners promoting tumors which proliferates carcinogenic substances.

The toxicant also alters reproductive and thyroid systems and functions of both sexes thus predispose them to diabetes, and cardiovascular diseases (Larry & Hansen, 2001).

PCBs are carcinogenic, teratogenic and persist in the environment. The exposure limits for this toxicant mainly elaborates on the occupational exposure which is the concentration of the stuff personnel can sustain without any adverse effect. The recommended permissible level is eight hours daily or 40 hours a week.


Chromium is naturally occurring in rocks, soil etc and in various forms. Chromium III and VI are the most prevalent forms in the environment. The exposure pathways involve breathing air, eating contaminated food, drinking water and through dermal route. Levels in water and air are low but contaminated food is the prime route for the general population because chromium is present in vegetables, meat and fruits (Habeck, 2010).

Acidic foods in stainless steel containers may contain chromium. High-exposure levels are common in industries that deal in chromium compounds. Some occupations that may experience chromium exposure include; painters, battery makers, candle makers, dry and cement makers. Tobacco smokers can also be exposed because tobacco contains chromium.

Chromium usually enters water, air and soil in chromium III & VI forms (Habeck, 2010). Cr (VI) is the ion liable for several toxic effects, but some of the molecular destructions are attributed to other forms. Chromium VI can be reduced to Cr (III) and Cr (V) which is short lived, but is extremely reactive and dangerous. Form VI is a strong oxidizing agent and easily forms complexes and its Cr (V), which is a reducing agent, makes it toxic.

Chromium (VI) turns to Chromium (V) due to some enzyme actions and this leads to the clogging of kidney and lung capillaries. High exposures result to several point DNA mutations, damage to chromosomes and changes in protein oxidation.

High levels of Cr (VI) cause running and irritating nose, nosebleeds in the septum. It also affects the respiratory system, skin and weakens the immune system of the body (Habeck, 2010). Occupational health and safety administration allows eight hours exposure of 5mg of chromium six. The minimum contaminant level in drinking water is 100ppb.


Acrylamide is a white substance which is soluble in water. The toxicant has several routes of exposure including oral though not common in human beings. Inhalation and dermal is common in occupational exposures parenteral exposures through intravenous and subcutaneous administration are common in animal.

Mechanisms of toxicity after exposure involve production of distal axonopathy in human beings damaging peripheral nervous system as well as central nervous system. This mechanism interferes with the transport system to the axon. Acrylamide may also bind to the DNA which then interferes with the protein structure responsible for axonal functionalities.

It also decreases the concentration of noradrenalin after interfering with postsynaptic dopamine receptor (Sunahara 2002). The toxicant has both acute and chronic effects. Acute effects include seizures, decreased levels of consciousness, hypertension and respiratory distress syndrome.

Well known chronic effects include ataxia and weakness in skeletal muscle. The exposure limits of this toxicant vary from suspected route of exposure. The permissible level is 0.3mg/m3 of skin. Employees should be kept below the exposure limits of the airborne.

Toluene diisocyanate (TDI)

Toluene diisocyanate is uses to manufacture poly urethane foams and elastomers, and it is one of the extremely hazardous substances. It is liquid at room temperature with a pungent smell. The main route of exposure is inhalation though direct contact is also common in occupational exposures. Its vapor is gladly engrossed in the lungs resulting in irritation.

Direct contact cause eye and skin irritation though dermal absorption is sluggish. Ingestion is also possible which causes irritation to the lips and mouth cavity (ATSDR, 2008). The main mechanism of exposure is by inactivating tissue biomolecules because it is decidedly reactive.

When ingested it forms insoluble globules, which live long in the body. TDI is not easily distributed in the human body, but is instead reacts with contact tissues. Throughout covalent bonding the amino group undergoes some reaction thus inactivating protein. The odor threshold is 2.1ppm while the permissible levels as per OSHA limit is 0.02ppm (ATSDR, 2008).

Risk Assessment

Hazard identification: The site has many toxicants following past information about the activities of the two industries. The industrial wastes include chromium, TDI, PCBs and Acrylamide, both of which are human health hazards. Literature reveals that the listed substances have adverse health effects like cancers when respective exposures exceed limits.

Pungent smell also dominates the site, a sign of chlorine based substance, which too is dangerous to animals and plants health. Clear observation revealed possible hazards from the unmarked drums, heaps of dust and the draining of the toxicant into the stream.

The stream is used for irrigation and fishing and drinking water source is next to it. This poses a significant health hazard to the residents who depend on this necessary resource (Lu & Kacew, 2009).

Dose-response assessment: Depending on the available data there are high chances of the residents experiencing health conditions associated with the suspected toxicant. The exposure limits for PCBs, TDI and other toxicants is unusually low because they are banned substances.

The prevalence of the toxicant on the site is higher than the recommended permissible levels; hence residents are at high risk of conditions resulting from their exposures. Increase in dose and exposure result, in adverse health effects (Lu & Kacew, 2009).

The magnitude of exposure is exceptionally high in drinking water from the site, eating fish and vegetables from the site as well as breathing air around indicate high levels of exposure. The residents, therefore, have a high probability of getting diseases and conditions associated with the toxicant.

Exposure assessment: This is the extent of exposure to one or more toxicants. Following past information, the residents have been exposed to a greater extent. Drinking of water from the open source next to the site which accumulates toxicants shows high extent of exposure. The vegetables and other fruits harvested from the fields irrigated with the water running through the sites are a leading source of exposure.

The fish from the stream accumulates the toxicant from the site, thus finding their way into the human body (Gunnar, 2007). The dust from the site accumulates on the objects which come into contact with human skin thus exposing them. The air around the site contains fine dust, smoke and fumes from the site which finds their way into the human body through breathing.

Risk characterization: Considering hazard identification, dose evaluation and exposure assessment, there is a clear indication that the population around the site is at high risk of health conditions. There are high levels of exposure which will result into severe health outcomes (Lu & Kacew, 2009).

There is a high risk because the toxicants cause cancer, birth defects and other severe diseases. The estimated risk may not be real because people react differently to toxicants, so the residents may show different conditions. The toxicants may be undergoing natural neutralization, hence may not cause anticipated health risks. There are inadequate data to conclude on the magnitude and nature of the risks.


The following recommendations are proposed to halt further exposures to the toxicants on the site. The site should be marked as a danger zone and the fence surrounded with warning messages about the heath risks of the toxicants on the site. Alternative source of water should be supplied to the local residents, since the current source of water contains persistent organic pollutants.

The residents should stop irrigation using water from the alleged stream, and fishing downstream; furthermore, health education should be intensified among the residents on the proposed actions. Experts in hazardous waste management should take immediate action as pertains to removing toxicants for safe and recommended disposal options thus eliminating future exposures (Duffus & Worth 2006).


Agency for Toxic Substances and Disease Registry (ATSDR). (2008). Medical Management Guidelines for Toluene Diisocyanate. USA.gov. Web.

Sunahara G. (2002). Environmental analysis of contaminated sites. Manchester: John Wiley and Sons.

Gunnar, N. (2007). Handbook of the toxicology of the metals, 3rd Edition. London: Academic Press.

Duffus J. & Worth, H. (2006). Fundamental Toxicology. Cambridge: The Royal Science of Chemistry.

Larry, W. & Hansen, L. (2001). PCBs: recent advances in environmental toxicology and health effects. Kentucky: Lexington, University Press of Kentucky.

Lu, F. & Kacew, S. (2009). Lu’s basic toxicology: Fundamentals, target organs and risk Assessment, 5th Edition. Washington, DC: Taylor & Francis.

Habeck, M. (2010). Toxicological profile for chromium. Eco-USA. Web.

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