Toxicological Concepts - Essay Example

Toxicological Concepts Name: Institution: Date: Introduction Occupational hygiene hazards are a threat to the health of employees at the workplace and they have to be traced through sampling. Individual workers have to be singled out for monitoring of the specific hazard. There are various sampling methods that are used to determine the level of concentration of the hazard at the workplace and they include grab sampling, continuous monitoring, long term monitoring, short term monitoring, and bulk sampling. Bulk sampling is essential for asbestos identification. Exposure standards are stipulated by Safe Work Australia in conjunction with the state governments. This essay explore occupational hygiene hazards by looking at their properties, toxicity, health effects, sampling and recommended exposure standards set by government agencies and hygiene organizations. Cadmium, arsenic, asbestos, lead and benzene have been discussed as most prevalent chemicals in Boiler manufacturing plant. Part 1 lists the hazards, route of entry into the body, state of matter and nature of exposure. Part 2 discusses properties, toxicity and health effect evidence while Part 3 exposure standards set various government agencies and occupational health organizations. Part 1 Occupational Hygiene Hazard State of Matter Route into the Body Nature of exposure (continuous/intermittent) 1 Lead Mists, vapours or fumes Through inhalation of the vapours, mists or fumes; ingestion of drink, food or dust/soil Continuous 2 Asbestos Fumes Through inhalation Continuous or intermittent 3 Arsenic Gas, fumes or dust Through inhalation and skin Continuous 4 Benzene Vapours Inhalation, ingestion and skin absorption Continuous 5 Cadmium Fumes or gas Inhalation Continuous Part 2: Properties, Toxicology and Health effects Lead Occupational exposure for lead happens through inhalation of lead-containing fume and dust and ingestion by coming in contact with lead-contaminated surfaces especially in the boiler manufacturing plant. Lead is referred to as a chronic toxin. It common to witness cases of a cute toxicity. Characteristics of acute lead toxicity comprise of dullness, GI disturbances, restlessness, poor attention span, irritability, headaches, renal and hepatic damage, hallucinations, and encephalopathy (Berlin, Yodaiken & Hanman, 2012). Prolonged exposure to lead causes haematological effects like basophilic stippling, anaemia, or neurological disturbances like irritability, headaches, convulsions, lethargy, ataxia, muscle weakness, paralysis and tremors. Chronic exposure to lead also may cause adverse effects on both female and male reproductive functions. Cardiovascular and renal toxicity can also be caused by prolonged exposure to lead. Lead absorption depends on the chemical and physical state of the metal, and is further influenced by physiological status, age, genetic factors, and nutritional status. Exposure to lead in the general public happens through oral route including inhalation. In the workplace setting, inorganic lead inhalation through fumes, mists as well as vapours is a main route of exposure (Silbergeld & Scherer, 2013). The toxicological effects are the same in spite of the route of exposure. Absorption of particulate lead due to inhalation includes deposition of airborne lead particles within the respiratory tract as well as clearance and absorption to the respiratory tract straight into the circulation. About 35% to 50% of inhaled lead with particles less than 1μm is usually deposited within the lower respiratory tract, in the alveolar tract, and 50-70% of an inhaled is absorbed (Paustenbach et al, 2010). Higher deposition levels may happen in course of larger particles but this usually happens in the upper respiratory tract and absorption takes place in the course of the ingestion route where small particles like those from exhaust fumes are absorbed completely. Gastrointestinal lead absorption is aided by the physicochemical properties of lead particles and by the physiological factors such as fasting, age, nutritional calcium as well as iron status or pregnancy (Hoffmann, 2012).. Route of absorption of lead has little impact on lead distribution. Lead is normally transported basically within the red blood cells usually attached on the plasma proteins. Lead that is absorbed is distributed through the blood into the mineralizing systems (teeth, bone) as well as plasma proteins. Bone accumulates lead through the human life span and concurrently lead is mobilized from bone through remodeling. Close to 90% of the total body burden of lead normally is found in the bone (Judson et al, 2009). In the course of chronic exposure lead becomes deposited within the form of insoluble lead phosphate in places of the skeleton that are growing rapidly like tibia, radius, tibia, and femur. Bone is usually mobilized to blood the effect that is most obvious in people with occupational exposure and older people. Asbestos Maim properties propelling the wide use of asbestos are mechanical strength, incombustility, thermal insulation, chemical strength, and low cost. Asbestos belongs to the amphibole and serpentine groups of rock-forming minerals and it is in fibrous form of mineral silicates. Commercial kinds that have been in use in Australia include serpentine, amphiboles and amosite. Chemicals in the boiler manufacturing industry may also contain asbestos that is harmful (Paustenbach et al, 2010). Activities that involves asbestos that require special attention in evaluation of exposure include asbestos demolition and removal work in buildings, boilers, power stations, and ships; maintenance workers such as computer cabling installers, electricians, air-conditioning installers where buildings are sprayed by asbestos. Inhalation of high levels of concentrations of asbestos may result in asbestosis which refers to progressive scarring of the lung tissue. May development of scar tissue can happen even after stopping of exposure. The impact of asbestos on plurae which is a thin membrane enveloping the lungs entails plaques, diffuse pleural as well as excess fluids (effusions) (Silbergeld & Scherer, 2013). Two major kinds of cancer associated with the asbestos inhalation include mesothelioma and lung cancer. Mesothelioma is cancer affecting pleura or the peritoneum and happen from brief moments of exposure together with a repeated exposure can lead to significant cumulative exposure. Arsenic Relative toxicity of arsenic compounds will depend on the chemical type, solubility, valence state [like As (V) or As (III)], and physical form. Soluble arsenic compounds such as sodium arsenite are more toxic as compared to insoluble compounds such as arsenic sulphide. Toxicity of arsenic trichloride, arsenic trioxide and trivalent arsenite is greater as compared to the pentavalent arsenate (Purser & McAllister, 2016). Arsine gas (AsH3) has clinical symptoms that are totally different from other arsenic compounds and is regarded as the most toxic arsenic compound. The route of entry into the body of inorganic arsenic is primarily through inhalation of arsine gas or arsenic dusts or fumes that are airborne. The size of particle of arsenic dictates whether arsenic will get access to lower respiratory tract or be transported to the upper airways and swallowed. Moreover, soluble forms of the inorganic arsenic compounds are absorbed well in the gastro-intestinal tract (approximately 60-90%) (Hartung, 2010). Some of the arsenic compounds are usually absorbed through the skin such as arsenic trichloride and arsenic acid. Inorganic arsenic cannot go over the blood-brain barrier but can cross the placenta hence extra precautions is needed for pregnant mothers when carrying out tasks involving arsenic. Acute clinical signs of arsenic exposure vary depending on the chemical state and type of the arsenic in place. Acute effects are as a result of short-term exposures as well as high concentrations of arsenic. Arsine gas is a haemolytic poison in acute and chronic exposures. Resulting jaundice can be very severe. Symptoms and signs of toxicity include diarrhoea, nausea, vomiting, apprehension, rapid heart rate, difficulty breathing, and malaise (a feeling of discomfort, uneasiness and being unwell) (Judson et al, 2009). Cases of acute kidney failure are common and usually fatal. Acute poisoning through arsenic compounds than arsine gas is rare in the industry but has happened due to inhalation as well as skin absorption together with ingestion. Arsenic can result into coma, convulsions, and death where there is severe poisoning. Exposure though oral ingestion of arsenic salts leads to acute gastrointestinal symptoms like abdominal pain and vomiting. Cardiovascular effects are manifested through vasodilation, cardiac depression and eventually shock. Some of the CNS effects include coma, headache, convulsions, and cerebral oedema. Peripheral nervous system sensory loss and motor dysfunction can happen one to three weeks following huge exposures to arsenic (Mercer, 2012). Chronic effects include conjunctivitis, mucous membrane irritation, contact dermatitis, blistering of the skin, scaling, loss of appetite, weakness, gastrointestinal disturbances, live diseases, destruction of the blood cells and damage to the nervous system. Benzene Work activities involving benzene include chemical manufacturing, handling petrol, plastic and rubber manufacturing, motor vehicle repair, steel production, firefighting, and refining operations. Acute exposure to high levels of concentration of benzene vapours can occasion irritation of the eyes, skin and respiratory system and within the central nervous system arrhythmias and depression (Purser & McAllister, 2016). Acute effects of high degree of benzene concentration can be narcosis, coma, unconsciousness and death. Usually Benzene concentration of approximately 20000 ppm is very fatal to human being within five to ten minutes. Exposures of 50 to about 150 ppm for several hours can lead to headache, vomiting, nausea, slurred speech, dizziness, fatigue, euphoria, irritability; weakness, loss of consciousness, disorientation, confusion and death. All organic solvents cause irritation of the respiratory tract to some extent due to the defatting action of solvents (Berlin, Yodaiken & Hanman, 2012). The irritation is normally reduced to the upper airways including sinuses and nose. Overexposure can lead to fluid accumulation in the lungs, or exacerbation of asthma. Upper respiratory tract irritation is characterized by sore throat and nose, cough and chest pain. Irritation of the eyes may happen if they are not protected by special vapour goggles. Chronic effects of benzene include bone marrow depression, leukaemia and destruction of red blood cells. Cadmium Work activities that may involve cadmium and its compounds exposure include welding, soldering, smelting, oxy-cutting, electroplating, use of cadmium-silver alloys, cadmium alloys manufacturing, and coming in conduct with cadmium powders. Non-work exposure of cadmium can happen through smoking (Hoffmann, 2012). Route of entry into the body is primarily though inhalation. Small particles of cadmium can be absorbed through the alveoli and the particles are commonly found in cigarette smoke as well as fumes. Acute effects of cadmium poisoning include inflammation of the lungs, severe tracheobronchitis, and fluid accumulation within the lungs. Mortality rate for acute pulmonary diseases is placed at 20% (Purser & McAllister, 2016). High ingestion exposure of cadmium salts that are soluble leads to gastroenteritis. Long-term workplace exposure to cadmium can lead to severe effects usually common in the kidneys and lungs. Cadmium exposure has been associated with chronic obstructive airway disease. Part 3: Exposure Standards, Sampling and Government Agencies and Occupational Hygiene organizations Exposure standard is that exposure standard stipulated in the Workplace Exposure Standard for Airborne Contaminants. Breathing zone describes a hemisphere of 300 mm radius in front of a person’s face as well as measured from the midpoint of an imagined line joining the ears. Peak limitation is the peak or maximum airborne concentration of any substance that is determined over the shortest practicable period of time which does not go beyond 15 minutes. 8-hour Time-Weighted Average (TWA) is the average airborne concentration of a specific substance when it is calculated over eight-hour working day within a five-day working week (Hartung, 2010). Short-term exposure limit (STEL) is the airborne concentration of any substance obtained as time-weighted average within fifteen minutes. Airborne contaminants exposure standards are prescribed under WHS Regulations and Work Health Safety (WHS) Act. In the course of daily exposure to airborne contaminant exposure above TWA is permitted for very short periods as long as they are compensated for equal exposures below the exposure standard in the course of the working day (Hoffmann, 2012). Where there is a TWA and STEL standard, the STEL has to be observed. Atmospheric monitoring is using an appropriate as well as valid sampling and analytical technique to get an estimate of degree of airborne contaminants inhaled by employees. The outcome of the monitoring is then compared with the applied Safe Work Australia standard to determine if exposure to the substance of an employee is excessive. The outcome of atmospheric monitoring can only be compared directly to the standards of exposure if personal monitoring was performed within the breathing zone of the employee for a suitable period of time hence the sample is regarded as a representative of exposure (Mercer, 2012). Monitoring has to be done through taking personal samples of the employee within the breathing zone. Outcome of fixed or static position monitoring cannot be used as a manifestation of actual employee exposure to the substance. Fixed or static position monitoring can assist in evaluation of effectiveness of risk controls. Interpretation of the outcome of atmospheric monitoring has to be carried out by a competent individual such as safety professional or occupational hygiene professional since it needs excellent understanding of the exposure standards. The process of interpretation has to take into consideration working shifts that are longer than 8 hours, the possibility of skin absorption as well as the likelihood of exposure to other substances (Purser & McAllister, 2016). Occupational Health and Safety Regulations 2007 (OHS) requires the atmospheric monitoring of a substance that is hazardous when the exposure standard for the substance is exceeded. The basic requirement of any measurement technique is that it has to be appropriate for the objective of measurement. It has to provide information need for decisions that will be made using the information (Hoffmann, 2012). Sampling or monitoring translates to the use of valid as well as suitable occupational hygiene techniques to come up with a quantitative estimate of exposure of employees to substances that are hazardous to human health. Grab or snap sampling can be applied as a screening technique. It gives the concentration of a contaminant during a specific time as well as a location and will assist to confirm presence and/or spot a suspected contaminant. Short-term monitoring determines concentrations over a short period of time usually up to 10 or 15 minutes. Results are calculated as time-weighted average (TWA) and it is fit to be compared with relevant recommended short-term exposure limits and quantify exposures. Long-term monitoring is also determined on a time-weighted average and relates to long term recommended limits (8 hour TWA). Continuous monitoring will show variations in concentrations and is the same as grab sampling to the extent that peak levels can be identified and average concentrations or exposures determined (Adami et al, 2011). Bulk sampling happens where bulk samples of the harmful substance may be taken and analyzed for purposes of identification. Bulk sampling is important in asbestos identification process. Asbestos Apart from the WHS regulations, there are specific requirements regarding the risk of exposure of airborne asbestos. It is stipulated under Regulation 420 that someone carrying out a business or undertaking a workplace to make sure that exposure to a person at the workplace to airborne asbestos is minimized or eliminated. This is not a requirement to an enclosed area in accordance with Regulation 477 (Conrad & Becker, 2011). TWA for asbestos is 0.1 asbestos fibre per milliliter of air over an eight-hour period. Bulk sampling is recommended for identification of asbestos. Arsenic compounds have the same target organ as asbestos. Health monitoring has to be performed where there is sufficient risk of exposure to the hazard and valid technique can be used to determine the effect on the health of the worker. Arsenic Arsenic and soluble compounds TWA is 0.05m/mg3. Arsine TWA is 0.05ppm and 0.16m/mg3. Arsenic requires both continuous monitoring and grab sampling to determine its concentration in the workplace and how is dangerous to the employees. Arsenic has same target organ as creosote (Conrad & Becker, 2011). Benzene Benzene TWA is 1ppm and STEL is 2.5m/mg3. Benzene can use short-term monitoring to keep in touch with its spread in the workplace. When determining the risks of exposure of contaminants within the working environment, the outcome of air sampling or the concentration measurement is compared with the Occupational Exposure Limits (OELs) (Purser & McAllister, 2016). The importance of monitoring is to find out the level of exposure to a worker. It is essential to carry out personal monitoring through attaching the monitoring device close to the breathing zone of the worker. Substances that can impact on the same target organ as benzene are chlorine compounds, isocyanates and cadmium. Cadmium TWA for cadmium and cadmium compounds is 0.01mg/m3. Short-term monitoring is recommended for cadmium due to the hazardous nature of the substance (Purser & McAllister, 2016). Special attention has to be taken in acute exposures to cadmium particularly high temperature processes that emit cadmium fumes. Cadmium has same target organs as lead compounds and thallium. Lead TWA for lead arsenate Pb3(AsO4)2 is 0.15m/mg3. Lead chromate standard value limit of exposure TWA is 0.05g/mg3. Lead, inorganic dusts as well as fumes TWA is 0.15g/mg3. There is no STEL prescribed for lead. Long-term monitoring is important for lead to tract its concentration at the workplace. Its chronic toxicity requires it is monitored continuously. Lead is commonly found in industrial areas as well as industrial chemicals used in firms (Silbergeld & Scherer, 2013). The workplace like the boiler manufacturing is more dangerous since it deals with metals and chemicals containing lead. Lead requires biological monitoring, physical examination, medical and occupational history in the course of its monitoring. Lead has the same target organs as mercury and toluene. Conclusion Cadmium, arsenic compounds, asbestos, lead and benzene are some of the hazards that can be encountered in a Boiler manufacturing plant. Their toxicity health effects are evident and it is important to monitor their concentration through sampling in order to make sure the recommended exposure standards are not exceeded. Adverse effects of these chemicals require that qualified persons be used to determine their level of concentration in the breathing zone of the employees. Occupational hygiene organizations’ recommendations have to be considered when handling these chemicals. High concentrations of these chemicals at the workplace are harmful to the health of workers. Continuous monitoring is required for the most harmful chemicals while short term monitoring is needed for the less harmful chemicals. The discussed chemicals are all harmful to the wellbeing of the worker and protective measures have to be taken into consideration. Chronic toxicity is common for lead and benzene. It is important to observe exposure standards set by government agencies and hygiene occupational organizations. References Adami, H.O.; Berry, S.C.; Breckenridge, C.B.; Smith, L.L.; et al. (2011). Toxicology and epidemiology: improving the science with a framework for combining toxicological and epidemiological evidence to establish causal inference, Toxicol Sci. 122: 223–234. Berlin, A., Yodaiken, R. E., & Hanman, W. A. (Eds.). (2012). Assessment of toxic agents at the workplace: roles of ambient and biological monitoring. Springer Science & Business Media. Conrad, J.W.; Becker, R.A. (2011). Enhancing credibility of chemical safety studies: an emerging consensus on key assessment criteria, Environ Health Perspect. 119: 757–764. Hartung, T. (2010). Evidence-Based Toxicology – the Toolbox of Validation for the 21st Century? ALTEX. 27 (4): 253–63. Hoffmann, S. (2012). Kick-off of the Evidence-based Toxicology Collaboration Europe, ALTEX. 29: 456. Judson, R.; Richard, A.; Dix, D. J.; et al. (2009). The toxicity data landscape for environmental chemicals, Environ Health Perspect. 117: 685–695. Mercer, T. (2012). Aerosol technology in hazard evaluation. Elsevier. Paustenbach, D. J., Finley, B. L., Lu, E. T., Brorby, G. P., & Sheehan, P. J. (2010). Environmental and occupational health hazards associated with the presence of asbestos in brake linings and pads (1900 to present): a “state-of-the-art” review. Journal of Toxicology and Environmental Health, Part B. Purser, D. A., & McAllister, J. L. (2016). Assessment of hazards to occupants from smoke, toxic gases, and heat. In SFPE handbook of fire protection engineering (pp. 2308-2428). Springer New York. Silbergeld, E.; Scherer, R.W. (2013). Evidence-based toxicology: Strait is the gate, but the road is worth taking, ALTEX. 30 (1): 67–73. Read More