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OHSE2640 Hygiene And Toxicology 1

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OHSE2640 Hygiene And Toxicology 1

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Course Code: OHSE2640
University: The University Of Newcastle

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1. Sources of exposure: Provide a summary of occupations/tasks that may present a risk of exposure and sufficient explanation of the processes to show how exposure can occur.2. Applicable Occupational Exposure limits (OELs / PELs): Provide the occupational exposure limits (OEL) applicable in Singapore. State if each OEL is long or short term and include any applicable skin or carcinogen notations.3. Toxico-kinetics: Provide an outline of how each substance can gain entry to the body, how and where it is distributed, pathways for biotransformation if it is metabolised, sites of accumulation or storage if appropriate, and pathways for its elimination from the body.4. Toxico-dynamics: Provide a brief description of how each substance (or its metabolite) can interact with cells and tissues to cause harm (mechanism of harm). Include a summary of the resulting health effects.5. Presentation & Referencing: Prepare the assignment using formal English and appropriate subheadings. Research the information in authoritative text and electronic resources, both in the library and on the internet, and reference appropriately. No specific referencing style is stipulated but be consistent and ensure that the appropriate forms for ‘in text’ citation and end listing of references are used.

Occupational Lead Poisoning
Several jobs are associated with lead poisoning as shown below:

Smelting or casting lead.

This entails the production of lead fume through secondary or primary smelting, in addition to lead foundries, and other operation such as recycling of scrap metal. Other synonym for this task is lead production which comprises of melting, pouring or refining lead. Smelting of lead produces lead fumes and dust that are inhaled directly through the respiratory system thus exposing the worker to lead related complications Balali-Mood et al. (1).

Removing of lead coatings

This includes thermal stripping or sanding of old paints through scraping, abrasive blasting, welding or torch burning. Lead exposure risk can also be encountered in occupations such as destruction of old structures, maintenance of steel bridge, painting of petroleum tanks, destruction of highway and railroad bridges and underground storage tanks, and commercial and institutional remodelling. The removal of lead coatings exposes the worker to lead poisoning through contact of the paint chips with the skin, exposure of lead dust to the skin, hair and respiratory system Lin et al. (2).

Heating, spraying lead products or machining

This poses risk of exposure to lead poisoning through the production of lead fume or dust generated by heating, machining or spraying lead products. The specific tasks in this category include repairing of the radiator or battery, welding, grinding lead alloys. Repair and extraction of water lines or cast iron soil pipes. Splicing and resplicing of electrical cables, molten lead spraying, firing ammunition, and removal and renovation of stained glass window Grover et al. (3).

Production of lead products

The manufacture of lead products include tasks such as the manufacture of lead-acid battery and glaze; making of lead-glazed pottery, manufacture of crystal glass, production of lead joints, cables, pewter, stained or leaded glass, paint and ink, leaded plastics. Mixing and weighing of lead powders, manufacture of ammunition and electric appliances such as ceramic coated capacitors and resistors Meyer et al. (4).
Occupational Exposure Limits applicable in Singapore
The Singapore Statutes Online (5) Permissible exposure level of lead under the first schedule is as follows:
Long-term PEL
Lead, inorganic dusts and fumes, as Pb – 0.15 mg/m3b
Lead arsenate – 0.15 mg/m3b
Lead chromate as Pb -0.05 mg/m3b
 and as Cr – 0.012 mg/m3b
Toxico-Kinetics of Lead
Lead enters into the body from the environment in different forms through inhalation, eating and drinking, and through the skin. The absorption of lead is reliant on a number of factors such as the physical form of lead, absorbed particle size, the transit time of the GI, and the well-being status of the person. More importantly, there is an inverse proportion between the particle size of lead and its absorption. Smaller particles are easily ingested.

Lead absorption through inhalation

Most of the lead used today enters the body through inhalation (breathing). When lead is scattered in the air in the form of dust or mist, it is easily inhaled and absorbed through the lungs and the upper respiratory tract. The leading source of occupational lead absorption is through inhalation of airborne lead Meyer et al. (6). The amount of lead absorption through inhalation is dependent on the size of the lead particle, the volume of the patients respiratory, the amount of deposition, and the mucociliary clearance of the inhaled lead.

Lead absorption through eating and drinking

Lead absorption through ingestion occurs when one handles lead containing items such as make-ups and then goes ahead and consumes food without proper hand washing. Once it gets through the mouth and swallowed, lead is absorbed through the digestive system causing various gastrointestinal tract complications Laidlaw et al. (7).

Lead absorption through the skin

Lead absorption through the skin is limited with less than one percent cases being reported. Lead dust or particles can enter via the skin if it is broken. An example of lead that can go through the skin is inorganic lead Ritchey et al. (8).
Distribution of lead
Most of the lead that is absorbed through inhalation or ingestion gets directly into the blood stream. Once lead is in the blood stream, it is circulated throughout the body and stored in different body tissues and organs Jones et al. (9). Some of the lead that is not stored is rapidly sieved and out of the body and excreted. The absorbed lead which is not eliminated from the body is exchanged mainly through three elements: blood, mineralizing tissues (bone and teeth), and soft tissue (brain, spleen, muscles, heart, liver and kidneys).


Lead enters the blood compartment immediately after absorption. Lead in the blood is mainly located within the red blood cells (RBCs). Only a little portion of the total lead burden is carried by the blood, nevertheless, it serves as the first recipient of absorbed lead and spreads it throughout the body, making it reach other body tissues or for elimination as waster products Khan et al. (10).

Soft tissue

The movement of lead in and out of the tissues is rapid, and it is distributed to various organs and tissues through the blood. Studies conducted on animals show that the liver, lungs and kidneys have the highest concentrations of soft-tissue lead straightaway after severe exposure. The brain is also a compartment of distribution. The study by Ragan et al. (11) prevention of lead poisoning in children indicated that adults retain less amounts of lead in soft tissue that children. The approximate half-life of lead in soft tissues is 40 days, and selective brain build-up may take place in the hippocampus.

Mineralizing tissue

A greater amount of lead absorbed and retained in the human body ends up being deposited in the bones. Over 90% of the total lead body burden is contained in the bones and teeth of adults, whereas, 75% is contained in children. There is also irregular distribution of lead in mineralizing tissues, with most of the concentrations occurring in bone regions especially those undergoing the most active calcification during exposure Gangoso et al. (12).


Most of the lead absorbed into the body is eliminated through renal clearance or through biliary clearance in the excrete. The quantity of lead eliminated and the time of excretion is determined by various factors. Colossal decline in ones BLL may require more months or even years, despite of the total elimination of the sources of exposure. It has been approximated that half-life of lead elimination in adults is 30 days, while in children it can go up to ten months Rastogi (13).
Toxico-dynamics of Lead
The toxicity of lead is notably as a result of its ability to mimic Calcium and substitute it in most of the primary cellular processes that rely on calcium Busse (14). Lead penetrates the cell membrane if different ways. Lead movement through the erythrocyte membrane is facilitated by the anion exchanger in a singular direction and via the Ca-ATPase pump in the opposite direction. Lead penetrates the cell membranes in other tissues through voltage-dependent or other forms of calcium channels. After lead has permeated the cytoplasm, it progresses its disparaging mimicking action by inhabiting the calcium binding sites on most of the proteins that are calcium-dependent. Lead binds to calmodulin which is a type of protein found in the synaptic terminal and operates as a sensor of free calcium accumulation and as an intermediary of neurotransmitter secretion. Additionally, it modifies the role of the protein kinace C enzyme, a fundamentally universal protein significant in most of the physiological functions.  The triggered kinase also impacts the expression of the Immediate Early Response Genes. Lead can also trigger gene expression through a mechanism triggered by protein Kinase C and it is suggested that this impact may be associated with modifications in synaptic functioning.
Through the capacity of lead to mimic calcium, lead is deposited in the bones and becomes a complete component of the bone, especially in cases of inadequate intake of calcium. Different psychological states of stress (such as breastfeeding, pregnancy, and diseases) can mobilise the deposited lead and is transported back to the blood stream, and also as a result of high intake of calcium in the diet. The stable condition of the lead in bones slows done recovery from lead poisoning, even when the toxic lead has entirely been removed (14).
As a result of the continuous presence of lead in the blood, all tissues are essentially damaged, especially the kidneys and the immune system. The harm caused to the nervous system due to lead poisoning is the most dangerous one. Lead poisoning in adults causes peripheral neuropathy, mainly featured by demyelination of the nerve fibres. Extreme exposure to high levels of lead leads to encephalopathy characteristic of insomnia, vertigo, migraine, convulsions, and even death. Reduces levels of lead triggers increased lead-induced neuropathy, which predominantly impacts the growing brain and aggravates difficulties in behaviour and cognitive impairment. Studies in epidemiology have indicated a significant relation between levels of lead in the blood and bones and poor outcomes in psychometric tests Rosin (15). A comparable association has also been evidenced in behavioural studies experimented on animals which had been exposed to lead immediately after birth (12). The process of learning is premised on the establishment and remodelling of synapses, and the toxicity of the metal on this process indicates that lead categorically damages the synaptic function. Nigg (16) shows that the rate of lead uptake on the blood-brain 2 into the brain occurs at a very high speed. The damaging effects of mental retardation and cognitive deficit caused by lead on the brain is attributed to its alteration of three primary neurotransmission systems namely glutamatergic, the dopaminergic, and cholinergic systems.
Sources of Exposure

Exposure to harmful levels of CO include:
The use of poorly maintained or heating appliance that is unvented.
Buildings or houses on fire
Heating the home using a gas stove, oven or grill
In appropriately vented natural gas appliances such as stoves or water heaters
Driving vehicles in enclosed spaces such as garages
Proximity to engine exhaust outlets
Using a camp stove, heater, or light with in a tent
Blocked heating exhaust vents or clogged chimneys
Running gas powered machines or generators indoors without enough air circulation
Industrial employees working at pulp mills, steel foundries, and the production of formaldehyde Weaver (17).

Co is formed as a by-product of consuming organic compounds. Insufficient oxygen inhibits the complete conversion of CO to carbon dioxide which is not poisonous. Hence, the reason why exposure cases of CO takes place in private residences where the combustion of organic compounds occurs in poorly ventilated spaces with reduced amount of oxygen (17). When inhaled, toxic CO impairs the delivery of oxygen and utilization at the cellular level. Low levels of oxygen in the blood will impair all organs especially the brain and heart which have the highest demand for oxygen. The characteristic affinity of CO to reversibly bind haemoglobin makes it work very fast, and as a result major body organs will lack enough blood supply causing relative functional anaemia with onset symptoms such as nausea, headaches, and fatigue (17).
Occupational Exposure Limits applicable in Singapore
Long-term PEL (5)
Carbon monoxide – 25 ppma    and 29mg/m3b        
Toxico-kinetics of Carbon Monoxide
CO gains entrance into the body through inhalation (mouth and nose) and to the lungs then readily absorbed into the blood unchanged and then distributed throughout the whole body.  The movement of carbon monoxide to the Hb-binding site is achieved through two procedural phases: transfer of CO in the gas phase, between alveoli and the airway opening, and the movement in the dissolved step, across the interface of air-blood.  The mechanisms of movement in the gas phase include physical action of the respiratory system and the cellular diffusion within the alveoli. On the other hand, the mechanism of the liquid phase involves the diffusion of carbon monoxide across the obstruction in alveolar-capillary, red blood cell (17).
The transportation of CO up to the Hb-binding sites involves its movement across the alveoli-capillary membrane, through the plasma via diffusion, permeation across the membrane of the red blood cells (RBC), and ultimately the stroma of RBC before the commencement of the reaction between CO and Hb. The Fick’s firs law of diffusion is a fitting example of a physicochemical law that governs the movement of molecules across the blood phase and membrane. The interchange and gas balance between air and blood takes place very fast. This movement is hastened by a partial pressure differential of CO across this membrane. For instance, an intake of air comprising of elevated CO levels through inhalation will quickly increase blood COHb. Through the instant and forceful binding of CO to Hb, CO’s partial pressure is maintained low, leading to an elevated accumulation variance between blood and air, and subsequently CO diffusion into blood. Continued breathing in of air free of CO will increasingly lower the gradient to its reversal point (elevated CO pressure on the blood side than alveolar air) and then there will be release of CO into alveolar air. Due to the strong biding of CO to Hb and substantially rapid reaction than CO elimination by ventilation, the concentration gradient of air-blood is normally higher than the gradient of blood-air, and the uptake of CO will be an equivalently quicker process than the clearance of CO (17).
The diffusion of CO is reliant on ventilation and the position of the body. In restful supine position, the diffusion of CO may be substantially higher compared to a restful sitting position. In both scenarios, the diffusion of CO during exercise is much higher than at rest Pendergast et al. (18). Diffusion rate of CO will rise with the increase of exercise. The elevation is as a result of the rise in both the pulmonary capillary blood flow and membrane-diffusing element Cotes et al. (19). The lung volume does not affect the diffusion of CO within the mid-range of crucial capacity. Nevertheless, the variation in rates of diffusion could be momentous in extreme volumes; at full lung capacity, the diffusion is much higher than normal, whereas at residual volume its level is lower than normal (17).
The rate of elimination of carbon monoxide from a state of equilibrium will take a monotonically declining, second-order function Goldstein (20). However, the elimination rate might not be uniform due to transitory exposures to CO, in which the equilibrium state may not be attained at the end of exposure. In such a scenario of intermittent high exposures of CO, it is likely that the decrease in COHb could be biphasic, and can best be estimated by a double exponential function. The opening decline rate or distribution may noticeably be rapid than the final phase of elimination Motterlini et al. (21). Studies have shown a decreasing divergence of CO in blood and exhaled air, an indication that the rate of CO elimination from extravascular pools are slower compared to those shown for blood Daher et al. (22). However, (21) notes that the total rates of elimination seem to be autonomous of the initial concentration of COHb.
Toxico-dynamics of Carbon Monoxide
Carbon monoxide is quickly absorbed into the lungs without being altered in anyway. Over 90% of the gas binds to haemoglobin after absorption, and approximately 10% to cytochrome C-oxidase and myoglobin. CO dissolved in plasma is below 1% and equally the same amount is oxidized to carbon monoxide.
Carbon monoxide binds with high affinity to several proteins containing heme. The affinity of Hb for CO is 250 times higher than for oxygen Hall (23). The oxygen carrying capacity is reduced due to the competition by CO for binding to Hb, and consequently oxygen displacement. The binding of CO to Hb leads to equilibration of the R-state (relaxed, high-affinity quaternary Hb state), increasing oxygen affinity of other sites in the tetramer of Hb, and further inhibiting the delivery and release of oxygen. The study by Hampson et al. (24) indicated that there is no direct correlation between clinical severity or clinical improvement of patients under CO poisoning with the elimination of COHb or with the level of COHb in the blood. The canine studies conducted by (20) indicate that the CO gas toxicity absorbed through inhalation is much higher than transfusion of the same accumulation of CO-exposed erythrocytes. The outcomes of the study points out the toxic impacts of CO outcomes from the world effect of CO inhibition on the delivery of oxygen alongside on the binding to cellular proteins containing heme.  Furthermore, CO binds to other proteins with heme such as skeletal muscle and myoglobin in heart.
The transportation of carbon monoxide in the entire body significantly shows the binding of carbon monoxide to heme proteins, for example myoglobin and Hb. The highest accumulation of total carbon monoxide ascertained from the tissues acquired from human autopsies were from the lung, kidney, spleen, and skeletal muscle, alongside noticeable levels in the adipose tissue and brain. On the other hand, the brain is significantly affected by carbon monoxide effects due to its rather high demand for oxygen. Increased levels of carbon monoxide in the skeletal muscle, blood, spleen, and heart is a reflection of the huge presence of carbon monoxide binding proteins in these tissues. Carbon monoxide while in blood, quickly spreads into erythrocytes in which it occurs majorly as a complex with Hb (COHb). When the gas exists in the muscle it majorly occurs as a complex with myoglobin (COMb). In the case of pregnant woman, the presence of the gas in the maternal system permeates to the fetal tissues in which it binds to the Hb of the fetal among other heme proteins.
Mitochondrion respiration is inhibited by CO through binding the ferrous heme a3 in the active part of COX, causing a total shut down of oxidative phosphorylation, just as cynide and nitric oxide behaves (24). The inhibition of COX slows down oxidative phosphorylation, causing a decline in the production of ATP in tissues such the heart and brain.
(1) Balali-Mood M, Shademanfar S, Moghadam JR, Afshari R, Ghassemi MN, Nemati HA, Keramati MR, Neghabian J, Balali-Mood B, Zare G. Occupational lead poisoning in workers of traditional tile factories in Mashhad, Northeast of Iran. The international journal of occupational and environmental medicine. 2010;1(1 January).
(2) Lin GZ, Peng RF, Chen Q, Wu ZG, Du L. Lead in housing paints: An exposure source still not taken seriously for children lead poisoning in China. Environmental Research. 2009 Jan 1;109(1):1-5.
(3) Grover P, Rekhadevi PV, Danadevi K, Vuyyuri SB, Mahboob M, Rahman MF. Genotoxicity evaluation in workers occupationally exposed to lead. International journal of hygiene and environmental health. 2010 Mar 1;213(2):99-106.
(4) Meyer PA, Brown MJ, Falk H. Global approach to reducing lead exposure and poisoning. Mutation research/reviews in mutation research. 2008 Aug 31;659(1):166-75.
(5) Singapore Statutes Online. Workplace Safety and Health (General Provisions) Regulations. Available from: https://sso.agc.gov.sg/SL/WSHA2006-RG1?DocDate=20110909&ValidDate=20160107&ProvIds=Sc1-#Sc1- [Accessed 14th Sep 2018].
(6) Meyer PA, Brown MJ, Falk H. Global approach to reducing lead exposure and poisoning. Mutation research/reviews in mutation research. 2008 Aug 31;659(1):166-75.
(7) Laidlaw MA, Taylor MP. Potential for childhood lead poisoning in the inner cities of Australia due to exposure to lead in soil dust. Environmental Pollution. 2011 Jan 1;159(1):1-9.
(8) Ritchey MD, Scalia Sucosky M, Jefferies T, McCormick D, Hesting A, Blanton C, Duwve J, Bruner R, Randolph Daley W, Jarrett J, Brown MJ. Lead poisoning among Burmese refugee children—Indiana, 2009. Clinical pediatrics. 2011 Jul;50(7):648-56.
(9) Jones RL, Homa DM, Meyer PA, Brody DJ, Caldwell KL, Pirkle JL, Brown MJ. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 years, 1988–2004. Pediatrics. 2009 Mar 1;123(3):e376-85.
(10) Khan DA, Qayyum S, Saleem S, Khan FA. Lead-induced oxidative stress adversely affects health of the occupational workers. Toxicology and Industrial Health. 2008 Oct;24(9):611-8.
(11) Ragan P, Turner T. Working to prevent lead poisoning in children: getting the lead out. Journal of the American Academy of PAs. 2009 Jul 1;22(7):40.
(12) Gangoso L, Alvarez-Lloret P, Rodríguez-Navarro AA, Mateo R, Hiraldo F, Donazar JA. Long-term effects of lead poisoning on bone mineralization in vultures exposed to ammunition sources. Environmental Pollution. 2009 Feb 1;157(2):569-74.
(13) Rastogi SK. Renal effects of environmental and occupational lead exposure. Indian journal of occupational and environmental medicine. 2008 Dec;12(3):103.
(14) Busse FP, Fiedler GM, Leichtle A, Hentschel H, Stumvoll M. Lead poisoning due to adulterated marijuana in Leipzig. Deutsches Ärzteblatt International. 2008 Oct;105(44):757.
(15) Rosin A. The long-term consequences of exposure to lead. The Israel Medical Association journal: IMAJ. 2009 Nov;11(11):689-94.
(16) Nigg JT, Knottnerus GM, Martel MM, Nikolas M, Cavanagh K, Karmaus W, Rappley MD. Low blood lead levels associated with clinically diagnosed attention-deficit/hyperactivity disorder and mediated by weak cognitive control. Biological psychiatry. 2008 Feb 1;63(3):325-31.
(17) Weaver LK. Carbon monoxide poisoning. New England Journal of Medicine. 2009 Mar 19;360(12):1217-25.
(18) Pendergast DR, Olszowka A, Farhi LE. Cardiovascular and pulmonary responses to increased acceleration forces during rest and exercise. Aviation, space, and environmental medicine. 2012 May 1;83(5):488-95.
(19) Cotes JE, Chinn DJ, Miller MR. Lung function: physiology, measurement and application in medicine. John Wiley & Sons; 2009 Apr 8.
(20) Goldstein M. Carbon monoxide poisoning. Journal of Emergency Nursing. 2008 Dec 1;34(6):538-42.
(21) Motterlini R, Otterbein LE. The therapeutic potential of carbon monoxide. Nature reviews Drug discovery. 2010 Sep;9(9):728.
(22) Daher N, Saleh R, Jaroudi E, Sheheitli H, Badr T, Sepetdjian E, Al Rashidi M, Saliba N, Shihadeh A. Comparison of carcinogen, carbon monoxide, and ultrafine particle emissions from narghile waterpipe and cigarette smoking: Sidestream smoke measurements and assessment of second-hand smoke emission factors. Atmospheric Environment. 2010 Jan 1;44(1):8-14.
(23) Hall JE. Guyton and Hall textbook of medical physiology e-Book. Elsevier Health Sciences; 2015 May 31.
(24) Hampson NB, Hauff NM. Risk factors for short-term mortality from carbon monoxide poisoning treated with hyperbaric oxygen. Critical care medicine. 2008 Sep.

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