Evaluating the Risk of Lung Cancer in Foundry Environments
VerifiedAdded on 2022/12/27
|9
|2076
|76
Report
AI Summary
This report assesses the risk of lung cancer among foundry workers, a significant concern due to the presence of carcinogenic chemical agents. The primary focus is on silica (SiO2), particularly crystalline forms, and polycyclic aromatic hydrocarbons (PAHs) like benzo[a]pyrene, both by-products of foundry processes. The report discusses the mechanisms through which these agents cause lung cancer, including silicosis and PAH-induced DNA damage and oxidative stress. It examines exposure limits, health guidelines, and treatment options, such as the use of Pembrolizumab for lung cancer. Additionally, the report emphasizes the importance of implementing control measures, like using alternative materials, improving ventilation, and regular health monitoring, to mitigate risks. The assessment also considers uncertainties in the scientific understanding and the evolution of foundry practices. The report concludes by highlighting the need for vigilant monitoring and control of emissions to reduce the incidence of lung cancer among foundry workers.
Contribute Materials
Your contribution can guide someone’s learning journey. Share your
documents today.

Running head: RISK OF LUNG CANCER IN FOUNDRY WORKERS
RISK OF LUNG CANCER IN FOUNDRY WORKERS
Name of the Student:
Name of the University:
Author Note:
RISK OF LUNG CANCER IN FOUNDRY WORKERS
Name of the Student:
Name of the University:
Author Note:
Secure Best Marks with AI Grader
Need help grading? Try our AI Grader for instant feedback on your assignments.

1RISK OF LUNG CANCER IN FOUNDRY WORKERS
Table of Contents
Introduction................................................................................................................................2
Discussion..................................................................................................................................2
Chemical Agent: Silica (SiO2)...............................................................................................2
Chemical Agent: Polycyclic Aromatic Hydrocarbon (PAH).................................................3
Guidelines..................................................................................................................................5
Silica exposure.......................................................................................................................5
PAH exposure........................................................................................................................5
Treatment...................................................................................................................................5
Conclusion..................................................................................................................................6
References..................................................................................................................................7
Table of Contents
Introduction................................................................................................................................2
Discussion..................................................................................................................................2
Chemical Agent: Silica (SiO2)...............................................................................................2
Chemical Agent: Polycyclic Aromatic Hydrocarbon (PAH).................................................3
Guidelines..................................................................................................................................5
Silica exposure.......................................................................................................................5
PAH exposure........................................................................................................................5
Treatment...................................................................................................................................5
Conclusion..................................................................................................................................6
References..................................................................................................................................7

2RISK OF LUNG CANCER IN FOUNDRY WORKERS
Introduction
Respiratory cancer has been a major concern among workers of heavy industries worldwide.
Production of iron and steel-based materials has increased exponentially with global inflation
of population and utility of metallurgic components have contributed into it. Several
components like silica, cadmium, polycyclic aromatic hydrocarbons (PAH) have emerged in
greater concentration than ever before as a principal by-product of these industries. Labourers
are the most exposed and in incessant contact with these toxic chemicals frequently
developing variety of diseases like lung cancer, cancer of the urinary tract, hepatic cancer and
several others. All of these chemical agents are recognized as carcinogenic by International
Agency for Research on Cancer (IARC) and emissions should be regulated within limits.
Discussion
Chemical Agent: Silica (SiO2)
Iron foundries are the principal producer of silica. In environment, silica is present in the
form of silicon dioxide (SiO2) and can be of two types-amorphous and crystalline.
Crystalline silicon dioxide is the most abundant form of silica emanated by foundry
industries, which has a diameter of <10μm. Such small-sized particles can easily pass
undetected through the primary barrier of human respiratory system (nasal hair, the pharynx)
reaching directly to the lungs. Prolonged exposure to SiO2 results in several types of silicosis,
tuberculosis, mycobacterial infection, progressive massive fibrosis (PMF) in foundry workers
[1].
In 2012, International Agency for Research on Cancer (IARC) had mentioned crystallized
silicon dioxide or quartz as a potential compound, which needs refocus for evaluating
Introduction
Respiratory cancer has been a major concern among workers of heavy industries worldwide.
Production of iron and steel-based materials has increased exponentially with global inflation
of population and utility of metallurgic components have contributed into it. Several
components like silica, cadmium, polycyclic aromatic hydrocarbons (PAH) have emerged in
greater concentration than ever before as a principal by-product of these industries. Labourers
are the most exposed and in incessant contact with these toxic chemicals frequently
developing variety of diseases like lung cancer, cancer of the urinary tract, hepatic cancer and
several others. All of these chemical agents are recognized as carcinogenic by International
Agency for Research on Cancer (IARC) and emissions should be regulated within limits.
Discussion
Chemical Agent: Silica (SiO2)
Iron foundries are the principal producer of silica. In environment, silica is present in the
form of silicon dioxide (SiO2) and can be of two types-amorphous and crystalline.
Crystalline silicon dioxide is the most abundant form of silica emanated by foundry
industries, which has a diameter of <10μm. Such small-sized particles can easily pass
undetected through the primary barrier of human respiratory system (nasal hair, the pharynx)
reaching directly to the lungs. Prolonged exposure to SiO2 results in several types of silicosis,
tuberculosis, mycobacterial infection, progressive massive fibrosis (PMF) in foundry workers
[1].
In 2012, International Agency for Research on Cancer (IARC) had mentioned crystallized
silicon dioxide or quartz as a potential compound, which needs refocus for evaluating

3RISK OF LUNG CANCER IN FOUNDRY WORKERS
carcinogenic toxicity [2]. According to Work Health and Safety Act, Australia, exposure to
crystalline silica should not exceed 0.1mg/m3 in workers of an industrial organization [3].
Silicosis is a potent life-threatening disease caused by quartz exposure. Various amounts of
silica exposure determine effective exacerbation of the disease.
Low to moderate exposure for more than 20 years can result classical silicosis in an affected
individual [4]. A pattern of circular opacity (1-10mm) in lung radiography is a typical sign of
classical silicosis. Acute silicosis is another form of severe silicosis where extremely elevated
levels of silica exposure cause complete disruption of the pulmonary function and results in
death [5]. Individuals having a tendency of smoking are likely to develop silicosis, those with
previous history of silica exposure. Computed Tomography (CT) could be performed to
screen the prevalence of lung cancer in a person.
Study [6] involving Turkish ceramic workers suggests, exposure to silica increases oxidative
stress in cells, with a lower expression level of catalase (CAT), glutathione peroxidise (GPx),
superoxide dismutase (SOD), while an increased level of malondialdehyde (MDA) and
glutathion reductase (GR) clearly attributing to higher levels of oxidative damage. Also an
increase in cytokine levels such as IL-1α, IL-1β, IL-2, IL-4, IL-6, IL-10, and TNF-α implies
imbalance in redox equilibrium and possible indications of inflammatory response.
Chemical Agent: Polycyclic Aromatic Hydrocarbon (PAH)
Polycyclic aromatic hydrocarbons (PAHs) are major by-product of incomplete combustion in
aluminium, automobile, iron, steel, copper and numerous other heavy industries. These are
lipophilic, non-polar compound, which are produced via partial combustion of organic
materials or biomass, petrochemical products [7]. Benzo[a]pyrene is the most common form
of PAH derived from this process and is used as a carcinogenic marker [8].
carcinogenic toxicity [2]. According to Work Health and Safety Act, Australia, exposure to
crystalline silica should not exceed 0.1mg/m3 in workers of an industrial organization [3].
Silicosis is a potent life-threatening disease caused by quartz exposure. Various amounts of
silica exposure determine effective exacerbation of the disease.
Low to moderate exposure for more than 20 years can result classical silicosis in an affected
individual [4]. A pattern of circular opacity (1-10mm) in lung radiography is a typical sign of
classical silicosis. Acute silicosis is another form of severe silicosis where extremely elevated
levels of silica exposure cause complete disruption of the pulmonary function and results in
death [5]. Individuals having a tendency of smoking are likely to develop silicosis, those with
previous history of silica exposure. Computed Tomography (CT) could be performed to
screen the prevalence of lung cancer in a person.
Study [6] involving Turkish ceramic workers suggests, exposure to silica increases oxidative
stress in cells, with a lower expression level of catalase (CAT), glutathione peroxidise (GPx),
superoxide dismutase (SOD), while an increased level of malondialdehyde (MDA) and
glutathion reductase (GR) clearly attributing to higher levels of oxidative damage. Also an
increase in cytokine levels such as IL-1α, IL-1β, IL-2, IL-4, IL-6, IL-10, and TNF-α implies
imbalance in redox equilibrium and possible indications of inflammatory response.
Chemical Agent: Polycyclic Aromatic Hydrocarbon (PAH)
Polycyclic aromatic hydrocarbons (PAHs) are major by-product of incomplete combustion in
aluminium, automobile, iron, steel, copper and numerous other heavy industries. These are
lipophilic, non-polar compound, which are produced via partial combustion of organic
materials or biomass, petrochemical products [7]. Benzo[a]pyrene is the most common form
of PAH derived from this process and is used as a carcinogenic marker [8].
Secure Best Marks with AI Grader
Need help grading? Try our AI Grader for instant feedback on your assignments.

4RISK OF LUNG CANCER IN FOUNDRY WORKERS
Presence of polycyclic aromatic hydrocarbons can be monitored through testing serum
samples, urinary tests of 1-HP (Hydroxypyrene) concentrations and breast milk components
of female during lactation [9]. 1.4 μmol 1-HP in per mole creatinine is the maximum
occupational exposure limit.
The carcinogenic activity of PAH is mediated by epoxidation via cytochrome P450 pathway.
PAH intercalates into the DNA of a cell, forming a DNA adduct, hence considered genotoxic
[11]. PAH can also exhibit detrimental effects by increasing oxidative damage and promoting
immunosuppression, including altered regulation or modification of epigenetic expression of
certain genes [10]. PAH toxicity associated with smoking behaviour, binge drinking further
enhances the adverse effects of these compounds. National Institute for Occupational Safety
and Health (NIOSH) has proposed a minimal detectable concentration of 0.1mg/m3 as an
emissive industrial limit for PAHs [15].
Recent study [10] on Mexican brick makers has found that PAH effects methylation of IL-12
and p53 gene. IL-12 is a cytokine produced by immune cells as a response to inflammation,
allergy and for differentiation of T-helper cells (TH1). Hypomethylation of IL-12 arise
inflammatory disorders and invasion of humoral and cell-mediated immune response, thus
compromising body’s immune system. In addition, PAH also promotes hypomethylation in
p53 gene, which is a master regulator of cell division. Thus by compromising the essential
p53 gene PAH induces uncontrolled growth of cells leading to cancer progression.
Presence of polycyclic aromatic hydrocarbons can be monitored through testing serum
samples, urinary tests of 1-HP (Hydroxypyrene) concentrations and breast milk components
of female during lactation [9]. 1.4 μmol 1-HP in per mole creatinine is the maximum
occupational exposure limit.
The carcinogenic activity of PAH is mediated by epoxidation via cytochrome P450 pathway.
PAH intercalates into the DNA of a cell, forming a DNA adduct, hence considered genotoxic
[11]. PAH can also exhibit detrimental effects by increasing oxidative damage and promoting
immunosuppression, including altered regulation or modification of epigenetic expression of
certain genes [10]. PAH toxicity associated with smoking behaviour, binge drinking further
enhances the adverse effects of these compounds. National Institute for Occupational Safety
and Health (NIOSH) has proposed a minimal detectable concentration of 0.1mg/m3 as an
emissive industrial limit for PAHs [15].
Recent study [10] on Mexican brick makers has found that PAH effects methylation of IL-12
and p53 gene. IL-12 is a cytokine produced by immune cells as a response to inflammation,
allergy and for differentiation of T-helper cells (TH1). Hypomethylation of IL-12 arise
inflammatory disorders and invasion of humoral and cell-mediated immune response, thus
compromising body’s immune system. In addition, PAH also promotes hypomethylation in
p53 gene, which is a master regulator of cell division. Thus by compromising the essential
p53 gene PAH induces uncontrolled growth of cells leading to cancer progression.

5RISK OF LUNG CANCER IN FOUNDRY WORKERS
Guidelines
Silica exposure
Usage of chromite or olivine sand as an alternative to silica.
Usage wet cleaning method or vacuum cleaners or providing adaptor components that
would bind to silica and reduce the amount of free airborne particles.
Mechanical handling in production to decrease exposure to silica and strictly avoiding
silica containing <2% moisture without proper safety equipments.
Implementing exhaust systems that will excavate sand dusts away from workers.
Regular monitoring of health issues should be encouraged by the PCBU.
PAH exposure
The affected worker should be immedietly removed from the working environment.
Concerning organization or PCBU should take swift action in remediation of the over.
The employee should be updated about his health condition after proper monitoring.
Treatment
Silica is a major component of our nature, found predominantly in the form of sand and rock
structures globally. Although, Silicosis is incurable, controlling silica exposure by
implementing detectors can help monitor occupational limits of 0.1 mg/m3 [3]. PCBUs
(Person conducting a business and undertaking) are responsible for providing primary
healthcare to the employers on hazardous exposure of chemicals. Treatment with synthetic
monoclonal antibody ‘Pembrolizumab’ can inhibit PD-1(Programmed cell death 1) - PD-L1
receptor-ligand interaction, facilitating cytotoxic T cell mediated antitumor activity in lung
cancer patients [12].
Guidelines
Silica exposure
Usage of chromite or olivine sand as an alternative to silica.
Usage wet cleaning method or vacuum cleaners or providing adaptor components that
would bind to silica and reduce the amount of free airborne particles.
Mechanical handling in production to decrease exposure to silica and strictly avoiding
silica containing <2% moisture without proper safety equipments.
Implementing exhaust systems that will excavate sand dusts away from workers.
Regular monitoring of health issues should be encouraged by the PCBU.
PAH exposure
The affected worker should be immedietly removed from the working environment.
Concerning organization or PCBU should take swift action in remediation of the over.
The employee should be updated about his health condition after proper monitoring.
Treatment
Silica is a major component of our nature, found predominantly in the form of sand and rock
structures globally. Although, Silicosis is incurable, controlling silica exposure by
implementing detectors can help monitor occupational limits of 0.1 mg/m3 [3]. PCBUs
(Person conducting a business and undertaking) are responsible for providing primary
healthcare to the employers on hazardous exposure of chemicals. Treatment with synthetic
monoclonal antibody ‘Pembrolizumab’ can inhibit PD-1(Programmed cell death 1) - PD-L1
receptor-ligand interaction, facilitating cytotoxic T cell mediated antitumor activity in lung
cancer patients [12].

6RISK OF LUNG CANCER IN FOUNDRY WORKERS
Bioremediation is one plausible method to degrade polycyclic aromatic hydrocarbons (PAHs)
from the environment [13]. Several Mycobacterium species has demonstrated to metabolize
PAHs and could be used for biodegradation of the compounds [14]. Catalytic converters
could be upgraded for lowering emission levels of PAHs in automobile industry [13]. Doctors
can prescribe creatinine test for an individual to detect PAH levels in their urine sample, as 1-
hydroxypyrene is the excretory metabolite of PAH. 1.4 μmol/ mol creatinine is the limit of 1-
OH which signifies that the worker has been exposed to excessive PAH, and should be
immediately removed from the environment [3]. The medical practitioner should also inform
the concerning PCBU for availing healthcare facilities for the patient and initiate reduction of
PAH emission in the workplace [3].
Conclusion
Chemical substances produced from foundry industries directly affect the workers. Most
common of them are quartz or crystalline silica in form of silica dioxide (SiO2) and
polycyclic aromatic hydrocarbon (PAH) in form of benzo[a]pyrene. Both of these compounds
exert severe health issues in daily labourers ranging from silicosis, mycobacterial infection,
tuberculosis, oxidative stress, inflammatory disorder, hypomethylation of regulatory genes,
disruption of chromosome structure-all of which could potentiate various types of cancer
including lung cancer. Treatment with pembrolizumab can exhibit beneficiary health
outcome in individuals with lung carcinoma. Monitored supervision of emission levels and
exposure for both silica and PAH could be a plausible solution to reduce the chances of lung
cancer occurrence in foundry workers.
Bioremediation is one plausible method to degrade polycyclic aromatic hydrocarbons (PAHs)
from the environment [13]. Several Mycobacterium species has demonstrated to metabolize
PAHs and could be used for biodegradation of the compounds [14]. Catalytic converters
could be upgraded for lowering emission levels of PAHs in automobile industry [13]. Doctors
can prescribe creatinine test for an individual to detect PAH levels in their urine sample, as 1-
hydroxypyrene is the excretory metabolite of PAH. 1.4 μmol/ mol creatinine is the limit of 1-
OH which signifies that the worker has been exposed to excessive PAH, and should be
immediately removed from the environment [3]. The medical practitioner should also inform
the concerning PCBU for availing healthcare facilities for the patient and initiate reduction of
PAH emission in the workplace [3].
Conclusion
Chemical substances produced from foundry industries directly affect the workers. Most
common of them are quartz or crystalline silica in form of silica dioxide (SiO2) and
polycyclic aromatic hydrocarbon (PAH) in form of benzo[a]pyrene. Both of these compounds
exert severe health issues in daily labourers ranging from silicosis, mycobacterial infection,
tuberculosis, oxidative stress, inflammatory disorder, hypomethylation of regulatory genes,
disruption of chromosome structure-all of which could potentiate various types of cancer
including lung cancer. Treatment with pembrolizumab can exhibit beneficiary health
outcome in individuals with lung carcinoma. Monitored supervision of emission levels and
exposure for both silica and PAH could be a plausible solution to reduce the chances of lung
cancer occurrence in foundry workers.
Paraphrase This Document
Need a fresh take? Get an instant paraphrase of this document with our AI Paraphraser

7RISK OF LUNG CANCER IN FOUNDRY WORKERS
References
1. Steenland K, Ward E. Silica: a lung carcinogen. CA: a cancer journal for clinicians.
2014 Jan;64(1):63-9.
2. on the Evaluation IW. SILICA DUST, CRYSTALLINE, IN THE FORM OF
QUARTZ OR CRISTOBALITE. InArsenic, Metals, Fibres and Dusts 2012. International
Agency for Research on Cancer.
3. Legislation.act.gov.au. (2019). [online] Available at:
https://www.legislation.act.gov.au/a/2011-35/default.asp.
4. Jalloul AS, Banks DE. The health effects of silica exposure. InEnvironmental and
occupational medicine 2007 (pp. 365-387). Lippincott Williams & Wilkins, Philadelphia, PA.
5. Levy BS. Wegman, DH. Baron, SL., Sokas, RK., editors. Occupational and
environmental health. 6.
6. Anlar HG, Bacanli M, İritaş S, Bal C, Kurt T, Tutkun E, Hinc Yilmaz O, Basaran N.
Effects of occupational silica exposure on oxidative stress and immune system parameters in
ceramic workers in Turkey. Journal of Toxicology and Environmental Health, Part A. 2017
Aug 3;80(13-15):688-96.
7. Rota M, Bosetti C, Boccia S, Boffetta P, La Vecchia C. Occupational exposures to
polycyclic aromatic hydrocarbons and respiratory and urinary tract cancers: an updated
systematic review and a meta-analysis to 2014. Archives of toxicology. 2014 Aug
1;88(8):1479-90.
8. Straif K, Baan R, Grosse Y, Secretan B, El Ghissassi F, Cogliano V. Carcinogenicity
of polycyclic aromatic hydrocarbons. The lancet oncology. 2005 Dec 1;6(12):931-2.
References
1. Steenland K, Ward E. Silica: a lung carcinogen. CA: a cancer journal for clinicians.
2014 Jan;64(1):63-9.
2. on the Evaluation IW. SILICA DUST, CRYSTALLINE, IN THE FORM OF
QUARTZ OR CRISTOBALITE. InArsenic, Metals, Fibres and Dusts 2012. International
Agency for Research on Cancer.
3. Legislation.act.gov.au. (2019). [online] Available at:
https://www.legislation.act.gov.au/a/2011-35/default.asp.
4. Jalloul AS, Banks DE. The health effects of silica exposure. InEnvironmental and
occupational medicine 2007 (pp. 365-387). Lippincott Williams & Wilkins, Philadelphia, PA.
5. Levy BS. Wegman, DH. Baron, SL., Sokas, RK., editors. Occupational and
environmental health. 6.
6. Anlar HG, Bacanli M, İritaş S, Bal C, Kurt T, Tutkun E, Hinc Yilmaz O, Basaran N.
Effects of occupational silica exposure on oxidative stress and immune system parameters in
ceramic workers in Turkey. Journal of Toxicology and Environmental Health, Part A. 2017
Aug 3;80(13-15):688-96.
7. Rota M, Bosetti C, Boccia S, Boffetta P, La Vecchia C. Occupational exposures to
polycyclic aromatic hydrocarbons and respiratory and urinary tract cancers: an updated
systematic review and a meta-analysis to 2014. Archives of toxicology. 2014 Aug
1;88(8):1479-90.
8. Straif K, Baan R, Grosse Y, Secretan B, El Ghissassi F, Cogliano V. Carcinogenicity
of polycyclic aromatic hydrocarbons. The lancet oncology. 2005 Dec 1;6(12):931-2.

8RISK OF LUNG CANCER IN FOUNDRY WORKERS
9. Ramesh A, Kumar A, Aramandla M, Nyanda A. Polycyclic aromatic hydrocarbon
residues in serum samples of autopsied individuals from Tennessee. International journal of
environmental research and public health. 2015 Jan;12(1):322-34.
10. Alegría-Torres JA, Barretta F, Batres-Esquivel LE, Carrizales-Yáñez L, Pérez-
Maldonado IN, Baccarelli A, Bertazzi PA. Epigenetic markers of exposure to polycyclic
aromatic hydrocarbons in Mexican brickmakers: a pilot study. Chemosphere. 2013 Apr
1;91(4):475-80.
11. Lyon F. IARC monographs on the evaluation of carcinogenic risks to humans. Some
industrial chemicals. 1994;60:389-433.
12. Garon EB, Rizvi NA, Hui R, Leighl N, Balmanoukian AS, Eder JP, Patnaik A,
Aggarwal C, Gubens M, Horn L, Carcereny E. Pembrolizumab for the treatment of non–
small-cell lung cancer. New England Journal of Medicine. 2015 May 21;372(21):2018-28.
13. Abdel-Shafy HI, Mansour MS. A review on polycyclic aromatic hydrocarbons:
source, environmental impact, effect on human health and remediation. Egyptian Journal of
Petroleum. 2016 Mar 1;25(1):107-23.
14. Cerniglia CE. Recent advances in the biodegradation of polycyclic aromatic
hydrocarbons by Mycobacterium species. In The utilization of bioremediation to reduce soil
contamination: Problems and solutions 2003 (pp. 51-73). Springer, Dordrecht.
15. NIOSH (National Institute for Occupational Safety and Health); 2010. <http://www.
cdc.gov/niosh/about.html>.
9. Ramesh A, Kumar A, Aramandla M, Nyanda A. Polycyclic aromatic hydrocarbon
residues in serum samples of autopsied individuals from Tennessee. International journal of
environmental research and public health. 2015 Jan;12(1):322-34.
10. Alegría-Torres JA, Barretta F, Batres-Esquivel LE, Carrizales-Yáñez L, Pérez-
Maldonado IN, Baccarelli A, Bertazzi PA. Epigenetic markers of exposure to polycyclic
aromatic hydrocarbons in Mexican brickmakers: a pilot study. Chemosphere. 2013 Apr
1;91(4):475-80.
11. Lyon F. IARC monographs on the evaluation of carcinogenic risks to humans. Some
industrial chemicals. 1994;60:389-433.
12. Garon EB, Rizvi NA, Hui R, Leighl N, Balmanoukian AS, Eder JP, Patnaik A,
Aggarwal C, Gubens M, Horn L, Carcereny E. Pembrolizumab for the treatment of non–
small-cell lung cancer. New England Journal of Medicine. 2015 May 21;372(21):2018-28.
13. Abdel-Shafy HI, Mansour MS. A review on polycyclic aromatic hydrocarbons:
source, environmental impact, effect on human health and remediation. Egyptian Journal of
Petroleum. 2016 Mar 1;25(1):107-23.
14. Cerniglia CE. Recent advances in the biodegradation of polycyclic aromatic
hydrocarbons by Mycobacterium species. In The utilization of bioremediation to reduce soil
contamination: Problems and solutions 2003 (pp. 51-73). Springer, Dordrecht.
15. NIOSH (National Institute for Occupational Safety and Health); 2010. <http://www.
cdc.gov/niosh/about.html>.
1 out of 9

Your All-in-One AI-Powered Toolkit for Academic Success.
+13062052269
info@desklib.com
Available 24*7 on WhatsApp / Email
Unlock your academic potential
© 2024 | Zucol Services PVT LTD | All rights reserved.