OBSERVATION - Shodhgangashodhganga.inflibnet.ac.in/bitstream/10603/43584/13/13_chapter_03.pdf · in...
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CHAPTER – III
OBSERVATION 1. FOUNDRY INDUSTRY AT KOLHAPUR AND WORK PLACE ENVIRONMENT
I) FOUNDRY INDUSTRY AT KOLHAPUR:
The spur of industrialization has given sudden flux of huge urbanization
with a vast need of infrastructural facilities. In this regard India has become one
of the major players in the developmental economy. Foundry industry shows
tremendous growth, both in volume and variety. In India large numbers of
foundries of all types are present. More than 95% of foundries are in small
sectors with wide variation in sizes, products, technology standards and work
culture. In India of all the foundry unit having installed capacity of approximately
7.5 million tones per annum amongst which around 95% of fall under small scale
industry category. India occupies a place of special importance in shaping the
Indian economy. A peculiarity of the foundry industry in India is the geographical
clustering. Each foundry cluster is known for catering to some specific end use
markets. Five major clusters in India are at Belgaum, Batala or Jalandher,
Coimbatore, Kolhapur and Rajkot.
India is the 6th largest producer of castings in the world after U.S, China,
Japan, Russia and Germany. India ranks 2nd next to China when global rank in
terms of operating units. The role of foundries and foundry technology has gone
up the by multifold meeting the demand from various sectors. Such as sugar
industry, agriculture and farm equipments and other metal oriented activities.
Foundry technology in India has made significant advancement during last
decade it gives direct employment to about 25% of all industrial labour
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Kolhapur is considered as the city of foundries number of renowned
industrialist has established foundries in Kolhapur. Various, small scale
industries have also started which are connected with foundries. Foundry
industry mainly produces castings which are required to automobile industry,
sugar industry, printing machines, agriculture and farm equipments, and various
other industries.
In Kolhapur foundry units were located, at three regions, MIDC Shiroli,
MIDC Gokul Shirgaon and in Udyam Nagar area. In Kolhapur about 60 foundry
units were present in which nearly 10,000 workers are working. The industry play
key role in the economy of our state. Thousand of male workers attend the
foundry work for 8-10 hours of the day.
2. WORK PLACE ENVIRONMENT:
In Kolhapur about 50 foundries units providing job to nearly 10,000
workers; located at three regions. In the heart of city small industrial sector is
present known as Udyam Nagar and other two regions are located near the
Kolhapur city in Shiroli MIDC and Gokul Shirgaon MIDC. The working conditions
in the foundries are quite adverse which affect the health and comfort of workers.
Generally in foundries major five sections are present which includes
Sand Plant, Fettling Section, Moulding Section, Furnace Section and Core Shop.
In these different sections variety of stresses affect health and comfort of
workers.
In Sand Plant sand moulds are commonly used for iron foundries. To
produce depression in the sand into which the metals was poured. In this section
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silica sand is mixed with coal dust and organic binders like bentonite powder or
dextrin. So sand reclamation and mixing is carried out in this section. Silica sand
brought from coastal areas like Vengurla, Fonda and from coastal regions of
Sindhudurg district, as well as coastal areas of Gujarat and Kattach. This sand
was light frown in color. All these components were mixed well the help of mixer
the molding sand from previous pouring was recycled, water and organic binder
are added before its use. In all this processes large amount of coal dust silica
dust is produced which spreads in working environment.
In Fettling Section activities which are carried out includes shot blasting,
fettling, chipping, and grinding. Due to these processes castings are cleaned and
dressed to remove any extra metal, sand, rough surfaces and other material
attached from molding processes. In shot blasting processes, castings are kept
in the shot blasting machine, and small steel shots or balls are strikes over
casting from all sides with high speed. So those castings are cleaned and all
adherent sand is removed. In this process large amount of silica dust and coal
dust is produced in the working environment. During grinding, fettling and
chipping rough and unwanted surfaces of castings become smooth and clean.
But in all these processes high intensity sound and metal dust is produced,
which leads to eye irritation and hand injuries like cut. Injuries due to manual
handling of material and castings are also takes place. Grinding wheels used in
dressing results in hand injuries.
In Moulding Section mould making, casting, pouring, knock out and
decoring processes are carried out. In the process of mould making two half
portions of mould boxes are used, one is called as pattern box. In both the boxes
mixture of prepared sand is poured by automatic moulding machine as well as
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by workers with the help of shovel. Then sand is properly by rammed into it core
is kept properly. Both the portion of boxes which kept accurately, one above
other fixed with fastener. The box is passed forward for pouring the metal. While
making mold large amount of dust is produced. And workers have to work in
awkward body posture. During pouring hot splashes of molten metal bounce out
leading to burn injuries. The hot molten metal also irritates eyes of workers due
to radiant energy. While pouring toxic fumes are emitted from the gas vent.
In Furnace Section charging, melting slogging and refining processes are
carried out. For charging pig iron, C.I. scrap, steel, lime stone, coak etc are used
in proper combinations along with silicon, manganese chromium and inoculants.
The quantity of material depends upon capacity of furnace. Now a days in
majority of foundries electric arc furnaces are used for proper melting in terms of
molten metal, cost and fuel saving. In the foundries melting is started at a 9 A.M.
for proper heating and obtaining the required temperature from electric are
furnace 30-40 minutes are required. Melting of metal and temperature controlled
manually by a worker. The temperature required for melting metal is 14500c to
15000c. After getting proper temperature in the furnace slag from the molten
metal is removed. At the time of pouring entire furnace is lifted slowly which is
controlled by worker and then metal poured into laddle. The laddle is then
carried towards the respective mould boxes for pouring. Maintenance of furnace
includes cleaning of the furnace, removing the attached metal to furnace,
checking inner asbestos layer, electric cables, coils and sealing etc. In this
section workers comes in contact with intense radiant heat and different toxic
gases are also emitted in the foundry working environment.
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In Core Shop cores are made and inserted into the mould in order to
determine the internal configuration of a hollow casting. The core must be strong
enough to withstand the casting process but at the same time must not be too
strong as to resist removal from the casting during the knocking out stage. Core
mixture comprises sand and binders, to give necessary strength such as linseed
oil, dextrin is used. Cores are made from the core sand to which organic binding
agents are added. The processing of these traditional cores involves oven curing
or stoving. For curing various synthetic resins are used. Curing is achieved by
chemical reaction and heating the cores at temperature 2600c to 3000c for about
three to five minutes. Then core box was removed from the core furnace or
automatic core machine, and then baked cores are removed and kept for
cooling. Inner cavity of cores and outer margins with surplus materials are
removed and cores are finished. In the process of core making toxic fumes are
generated which are inhaled by workers, leading to irritation of throat, these
fumes also affects eyes leading to foggy vision.
Plate No. I-A and II-B shows working environment of different sections of
foundry. Workers are working in sand plant fettling section; moulding section,
furnace section and in core shop. In sand plants workers are without protective
equipment. In fettling sections workers are working in awkward body posture and
the work environment is dusty. In furnace section workers are working very close
to molten metal and without heat proof clothing and protective equipments.
Table No.1. Shows noise level observed in different sections of foundry.
In Fettling section molding section and furnace section noise level ranges from
74 dB to 105 dB. High intensity noise produced due to fettling activities like
grinding chipping, shot blasting and knockout processes. Table No.2 shows
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illumination level at different sections in foundry. The recorded level ranges from.
1000lux to 190lux. Illumination level was very poor in sand plant and moulding
section. Table No. 3 shows temperature recorded in different sections of foundry
which ranges from 24oC to 34.50C. Higher temperature recorded in furnace
section and core shop where furnace was used. Table No. 4 shows dust
concentration in different section of foundry which was sampled by Dust sampler
RDS-3. The average dust concentration recorded in different sections of foundry
ranges from 114 µg/m3 to 650 µg/m3dust concentration was highest in sand
plant,moulding section; fettling section and core shop and furnace section. The
different activities in each section produces large amount of dust which spreads
in working environment of foundry. Table No. 5 shows trace elements and its
concentration recorded in foundry dust. It was observed that in foundry dust
concentration of Ni is higher and it is up to 1.903 µg/m3 below that Fe; 0.594 and
Cu is 0.792 µg/m3.
3. FOUNDRY WORKER:
In the foundry industry, there are two categories of workers, permanent
workers and labor contract workers. All workers are all male. Foundry industries
of Kolhapur constitute about ten thousand workers. Foundry worker attend the
work place in different sections for at least 8 to 10 hours of the day. The work is
carried in three shifts i.e 8 A.M. to 4 P.M. 4P.M to 12 P.M. and 12 P.M. to 8 A.M.
the worker in foundry industry fall in the age group of 21 to 30 years and 31- 40
years and have worked for long periods of service up to 15 years.
In our previous study More and Sawant (2003) the questionnaire survey
revealed that most of the workers were illiterate, smokers, drinkers and earning
less money as compared to the efforts undertaken. Most of the workers have
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many complaints regarding health i.e. lower back pain, chest pain, pain in hands
and feet, eye irritation, vertebral dislocation, irritation in nose and problems in
vision, observations of occupation stresses in these foundry workers is that, due
to postural strain 37.8% workers complain about lower back pain 45.9% workers
complained about pain in hands and feet. Higher concentration of dust affect the
respiratory system and causes chest pain in 27 % workers and irritation in nose
in 35.1% workers.
The work place study shows that, higher concentration of dust, high
intensity noise, radiant heat near the furnace and vibrations are the main factors
which make the working environment stressful for workers.
Physical fitness score of the foundry workers suggest that only 2%
workers show very poor physical fitness score, 8.0% workers show low average,
2.0% workers show high average, 36.6 % workers show good physical fitness
score and 52% workers show excellent physical fitness score.
It was also observed that mean physical fitness score of foundry workers
gradually reduces according to period of work exposure.
The grip strength study of workers shows poor performance, due to
heavy work and duration of hours of work.
A significant observation in the present study was observed that, there is
a variation in the body temperature and pulse rate of foundry workers. It was
also observed that the systolic and diastolic blood pressure values were raised
according to work exposure. Mean values of blood pressure in control were
125.75 and 84.25mm Hg respectively, these values were elevated after work
exposure of above 15 years to 134.00 and 88.00mmHg. The respiratory
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functions also showed significant observations. Mean PEFR values were
decreased. The mean PEFR values of control were 547.49 but value was
decreased after work exposure above 15 years to 475.15. Tidal volume, IRV
values, ERV, VC, FVC, and FEV, values were found to be decreased. In sand
plant, core shop and molding section FEV, values are decreased. It was also
observed that total lung capacities of workers were significantly decreased as
period of work exposure increases mean IRV values of control was 0.984 l/min,
but after 15 year exposure it decrease up to 0.960 l/min. Mean ERV values of
control was 0.843 l/min, which was decreased up to 0.666 l/min after 15 years
exposure. Mean vital capacities of control was 2.367 l/min, which was decreased
up to 2.325 l/min after 15 years exposure. Mean TLC values of control was 3.565
l/min, but after 15 years exposure it decreases up to 3.525 l/min. Mean FVC
values of control was 2.009 l/min, which was decreased after 15 years of
exposure to 1.635 l/min. Mean FEV, values of control was 1.137 l/min, but after
15 year exposure it decrease up to 0. 715 l/ min.
Due to exposure in the foundry environment the hematological
parameters of foundry workers showed following observations mean
hemoglobin, concentration shows significant decrease in values. Percent
neutrophil also shows significant decrease in values. In fettling shop neutrophil
count was decreased. In other sections not much change was observed.
Eosinophils were found to be increased in sand plant and fettling shop, while no
significant change was observed in other sections of foundry. Basophil count is
increased in fettling shop. While no significant change was observed in other
sections. Monocyte and lympocytes were found to be normal. All parameters
chosen for determination of lung function status of workers are observed to be
on lower side as compared to those of controls. PEFR, FVC and FEV, values are
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found to be the most affected and more than 60% of foundry workers were found
to have respiratory impairments.
4. STRESSES IN FOUNDRY INDUSTRY:
Stress is discomfort caused by intrinsic or extrinsic factors called as
stressors, which produces charge in normal function of man, both physical and
mental. These effects of stress may be either reversible or irreversible.
Occupational stress can be defined as an additional stress on body and
mind, arising due to individuals occupation or employment.
Occupational stress is further divided into many types like, physical,
chemical, psychological, physiological etc. physical stress originates due to
muscular work which may be static or dynamic Various physical factors act as a
stressors, it includes dust, heat, illumination vibrations, excessive noise etc.
Chemical stress is caused due to chemicals used in various processes from
which toxic vapours, fumes and gases are released in working environment.
Mechanical stress is caused due to mechanical work, repeated cycles of same
work lead to stressful condition of workers. Workers also show psychological
stress. The questionnaire survey revealed that many workers have very low
wages, they have no job guarantee. Their relations with supervisors were not
good. Some workers also work under psychological stress also called as mental
stress. It is due to monotonous work. Mental stress can be observed due to
responsibilities and worries and as well as family relations of workers also have
to face physiological stress, due to musculoskeletal stress, it leads to stress on
different organ systems, like respiratory system, thermoregulatory system,
auditory system etc; some times workers have to face injuries and burns at the
work place.
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In the foundry operations, the workers are exposed to most of
occupational health hazards and stress factors. The occupational health hazards
in foundry can arise for example, due to sand mixer, high concentration of silica
dust, excessive noise, heat, metal dust, inadequate illumination, vibrations, risk
of burn injury due to molten metal and splashes, gases and vapors and other
manual operations may result a risk of physical injury to workers.
Dust from foundry shake out and returns sand handling system is
composed of sand particles, which are fractured by heat binders such as
bentonite, clay etc. Dust from casting, cleaning equipments such as shot blasting
machines, tumblers, vibrators and grinders contain all these particles and large
percentage of iron particles. Foundry environment also contain other irritants like
formaldehyde, isocyanates, various amines and phenols. These contaminants
are generated primarily by the core making and moulding processes and irritate
the eyes and respiratory tract.
The lung disease silicosis results from prolonged exposure to excessive
concentrations of repairable free crystalline silica dust. Dry sand is potentially
more hazardous. Metal dust is also associated with foundry operations like silica
it is toxic and harmful and leads to various skin complaints. It causes irritation
and damage to skin and eyes. It is not always visible and hence workers need
help to reduce possible danger to their health. In foundry the risk of accident or
disease is due to bad house keeping at the place of work.
The working environment in foundry is much noisy and damages not only
workers hearing but also their other organ systems like cardio- vascular and
nervous system. In the fettling shop noise is considerably higher, and workers
are exposed to noise level over 100db. Grinding and chipping tools used in
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dressing operations cause vibration induced health effects. Noise and vibrations
are other physical factors. Physical factors of working environment are so
important that they are delt within International Labor Organization Standards as
a separate subject. Workers are not always conscious to noise because they
easily become used to persistent noise and may not realize that it is doing them
harm, until it is too late to know.
In foundry operations formaldehyde, various resin products, hard woods
and acids associated with pattern making and core making processes which can
irritate the skin and precipitate allergic skin reactions.
Heat exchange takes place by convection, radiation, evaporation heat
transfer and conduction. As contact area between the skin and solid objects is
usually very small, conduction is negligible and it is discounted except in the
case of body cooling garments. Humidity and air movements modify the heat
load experienced by humans. The character of thermal environment is
determined not only by its total thermal energy content, but also by the flow of
thermal energy as a result of temperature differences. Human beings are
homeotherms, and are well equipped to live in wide range of environmental
conditions. The deep body temperature can not be allowed to fluctuate beyond a
relatively narrow range without leading to serious consequences to normal
functional efficiency.
Radiant heat is the major occupational hazard to the working
environment of the foundry. Heat radiates from heat sources and from molten
metal. Stress of heat affects health and is responsible for painful cramps,
fainting, heat exhaustion and heart stroke, this affecting the efficiency of workers.
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Frequent unprotected viewing of hot, molten metal in furnace and pouring areas,
cause eye cataracts.
In addition to dust, the air in foundries contains the other irritants like
formaldehyde, isocyanidates various amines and phenol. There contaminants
are generated primarily by the core making and molding processes and irritate
the eyes and respiratory tract. Vapors from various resins initiate severe allergic
reactions. Carbon monoxide gas was also produced due to thus possible
secondary effect of exposure is an increased risk of accident. Workers face
serious burns from splashes of molten metal in the melting and pouring areas of
foundry. Frequent unprotected viewing of hot, molten metal in furnace and
pouring areas causes eye cataracts. Eye injuries due to fragments of metal
occur in fettling shop injuries to the manual handling of materials and due to falls
also occur. Grinding wheels used for dressing small castings results in hand
injuries.
Silica exposure as a risk factor for scleroderma:
One of the significant observations noticed during this animal model study in
foundry environment is that of occurrence of systemic sclerosis in several
foundry workers. During physical examination of palms of foundry workers from
core shop (S 5) it was noticed that there are white spots on the palms and
particularly on finger tip of these workers and some fingers are slightly curved
(Fig. No. 1 and 2).
Among the potential risk factors for systemic sclerosis, occupational
exposures of silica have received very little attention. It was observed that skin
lesions starts at ventral side of the palms at certain locations particular more
significantly on the finger tips. Calcification occurs at these locations particularly
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in the pulps of the fingers (Fig. No. 2, 3 and 4). Involvement of skin on the palm
consists of dermal thickening through the process of fibrous replacement of
normal dermal structures. This thickening often extends in to the subcutis, and
leads to gradually increasing rigidity of the skin with tightening and atrophy of the
overlying epidermis. The fingers become hard, rigid, reddish and shiny (Fig. No.3
and 4). Subcutaneous calcification (Calcinosis cutis) can also be seen as white
spots on the ends of the fingers.
5. Exposure of an animal model:
Male albino rats were selected as experimental animal, divided into six
groups, each group of three animals. One group kept as control and other five
standard cases groups exposed in different sections of foundry for the period of
8 hours, 16 hours and 24 hours respectively.
On exposure in the different sections of foundry, the animals were found
to be under stress plate III shows animal exposure. In response to stress
animals exposed to various physiological responses. These responses are as
follows:
I. In all the cases of animals, after putting in the foundry sections, defecation
and urination was observed within 5-10 minutes.
II. Later the animal becomes very active and tries to escape out of the cage.
III. Animal started scrubbing nose, with front paws and after 15-30 minutes.
IV. All experimental animals become tired and showed deep breathing force
thing after 2 hours onward.
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V. Animal showed frequent drinking of water after 2 hour exposure, but animal
had not taken food. Large amount of Water was consumed by animals.
VI. As exposure period proceeds after 3 hours animal showed deep breathing
and goes into sleep. In some cases animals become very active and later
on become motionless and go into sleep.
VII. After 4 hours onward continuous exposure, frequent piloerection on skin
was observed.
VIII. In some cases animal show difficulty in breathing, and show oral
respiration but mostly in all cases scrubbing nose response is observed.
IX. After 5 hours of exposure in all cases food intake and frequent urination
was observed.
X. In core shop and furnace sections animal, sits on the wet surfaces in cage,
mouth and nose portion of experimental animal become reddish in color.
XI. Due to excess salivation mouth and nose area become wet. Animal cleans
face, ears and body frequently.
XII. In most of the cases after 6 hours animal shows sleepy posture. In plate III
fig 6 inverted sleeping postures was observed.
5. BEHAVIORAL CHANGES IN EXPERIMENTAL ANIMAL:
In pharmacology and other biosciences the measurement of animal activity
has been carried out. A change in spontaneous motor activity is an indicator of
animal response to central stimulants and depressants of therapeutic and
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toxicological importance Fig. No.2 shows block diagram of animal activity
monitor.
Fig. No. 3 show behavioral changes in animal recorded by “Animal Activity
monitor” in foundry environment. Table No. 6 shows responses of animal
recorded by Animal Activity Monitor Plate No.IV
It has been observed that, animal showed frequent activity to escape out,
and later on went to sleep and show sleepy posture. The maximum activity was
recorded in between 30 min to 50 min of exposure. In sand plant maximum
activity was recorded at 30 min and which was 20 beeps. In fetling section
maximum activity was recorded at 40 min and beeps recorded are 15. In molding
section maximum activity was recorded at 40 min and beeps recorded are 18
beeps. In moulding section, maximum activity was recorded at 40 min and beeps
recorded are 18 beeps. In core shop maximum activity was recorded at 50 min
and beeps recorded are 19. In the sleepy posture activity of animal reduced and
recorded as ‘0’ beeps.
6. NASAL LAVAGE:
Microscopic observations of nasal lavage smear of control rat shows that, the
nasal epithelial cell have prominent nucleus, cellular debris and mucus secreted
by mucus glands. In experimental group of rat nasal lavage smear shows
changes at cellular level, with heavy shedding of epithelial cells and mucus was
observed. In Plate V Fig. 3 large quantity of dust particles and mucus was
observed In Fig.4 there is necrosis of epithelial cell. Significant change was
observed in nasal lavage smear of rat is pikonotic nuclei, the fragmented nuclei
are visible in cytoplasm of epithelia cells. In Fig. 6 of plate V shows cellular
debris and dust particles.
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In comparison with control group of animal, the nasal lavage smear of
experimental animal show large amount of mucus shedding, exfoliation of
epithelial cells, cellular debris and trapped foundry dust particles were
significantly observed.
7. BRONCHOALVEOLAR LAVAGE (BAL):
The bronchoalveolar lavage smear study of control rat show, the smear
contains prominent epithelial cells, mucus material and cellular debris. [Plate VI.
Fig. 1] The bronchoalveolar lavage smear study up to 8 hours exposure reveals
that, the smear contain mucus material, cellular debris and appearance of
megakaryocytie and megakaryoblast Fig.2.
The number of megakaryocytie, megakaryoblast macrophages and dust
partials are increased after 16 hours exposure. It has been shown in Fig 3 and 4.
After 24 hours exposure the BAL smear shows appearance of
polymorphonuclear leulcocyte, megakaryoblest, megakaryocytic along with dust
particles. (Fig. 5 & 6)
Overall scenario of Bronchoalveolar lavage smear reveals that exposure to
foundry environment induces release of PMN (polymouphonuclear leukocytes),
macrophages, megakaryoblast and megakaryocytie cells in rat.
8. ORGAN HISTOPATHOLOGY:
a. Trachea:
Trachea is elongated tube starts from laryngopharynx and joins with lungs in
thoracic cavity. Histological transverse section of trachea shows four layers i.e.
innermost mucosa, submucosa or muscularis with muscle layer, hyaline cartilage
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and outer adventitia. The innermost layer is made up of pseudostratified ciliated
epithelial cells, below which is present a submucosa or muscularis layer in which
seromucous glands were scattered, which open into lumen of trachea. The
hyaline cartilage is ‘c’ shaped consist of matrix with many lacunae, these
lacunae occupied by chondrocyte or chondroblast cells. The hyaline cartilage is
surrounded by connective tissue adventitia. Fig. No.1 of plate VII shows T.S. of
trachea of control rat.
It has been revealed that, there is no change in the histological structure of
trachea upto 8 hours exposure to foundry environment, while mild thickening of
mucosa and hyaline cartilage observed after 16 hours exposure and up to 24
hours. Table No. 7 shows histopathological observations of T.S. of trachea.
Mild peritracheal edema observed after 16 hours exposure and it becomes
moderately severe after 24 hours.
Mild fibrosis below mucosa and surrounding the hyaline cartilage appears
after 24 hours exposure. Mild fibrosis of hyaline cartilage observed after 24 hours
exposure to foundry environment.
b. Histopathology of lungs:
Lungs are located in thoracic cavity and connected by trachea with the
help of bronchi. It plays an important role in gases exchange (02 and C02).
Histological transverse section of lung of rat consists of intrapulmonary bronchus,
terminal bronchioles, alveolar ducts, alveoli (air spaces), intraalveolar septum and
blood vessels. The structure of intrapulmonary bronchus have pseudostratified
ciliated columnar epithelium, smooth muscles in which seromucus glands were
scattered, hyaline cartilage and outer connective tissue adventitia. The terminal
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bronchioles have same structure except hyaline cartilage. The terminal bronchiole
later divided into alveolar ducts which communicate with alveoli. The intralaveolar
septum in which blood capillaries are embedded contain blood for exchange of
gases. The interalveolar septa or wall of alveoli i.e. alveolar epithelium constitute
of two types of cells i.e. Alveolar type I cell pneumocytes and Alveolar type II cell
pneumocytes. The Alveolar type I cell play significant role in removal of surfactant
produced by Alveolar type II cells. Alveolar type II cells have two important
functions i.e. it serves as a stem cell for production of alveolar type I cell and with
cytolysosomes it produces surfactants.
Fig. No.1 of plate VIII-A and VIII-B shows T.S. of lung of control rat
indicating, bronchiole, alveoli, normal thickness of interalveolar septum and blood
vessel.
Table No.8 shows histopathological changes in lung of rat on exposure to
foundry environment mild alveolar congestion reducing alveolar space observed in
T.S. of lung from 8 hours exposure to 16 hours exposure which later become
moderate after 16 hours exposure and severely moderate after 24 hours
exposure. (Fig No. 6 and 7 of plate VIII-A)
Mild thickening or alveolar wall was observed from 8 hours exposure which
become moderate after 16 hours exposure and later moderately severe in T.S. of
rat lung after 24 hours exposure respectively. Fig. No. 7 and 8 of plate VI Fig. No.
1, 3 and 4 of plate VIII-A.
The blood vessel showed no change up to 8 hours exposure but thickening
of wall of blood vessel was mild up to 16 hours exposure and moderate after 24
hours exposure in foundry environment. The lumen of wall of blood vessel
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completely reduced after 24 hours exposure. Fig. No.5 to 8 of plate VI, Fig. No. 3,
6 and 8 of Plate VIII-A.
Per bronchial edema was mild on 16 hours exposure and moderate after 24
hours exposure in foundry environment Fibrosis between bronchial wall and
Fibrosis in alveoli was mild after 24 hours exposure. Fig No. 6 and 7 of plate VIII-A
and Fig No. 2, 3 and 4 of plate VIII-B shows that, on 24 hours exposure to foundry
environment, there is significant alveolar congestion, red cell congestion,
thickening of blood vessel, peribronchial edema and fibrosis in wall of bronchi and
alveoli of lung.
c. Histopathology of liver :
The liver is one of the largest and most important vital and versatile organ in
the body, performing significantly essential functions and contributing to
homeostasis. By various estimates the liver performs as many as 500 different
functions. The liver work as storage depots for glucose, fats, iron, copper and
many vitamins. It synthesizes some key blood proteins involved in clotting and is
an essential detoxifier of potentially harmful substances.
Histologically, the liver is lobed and surrounded by connective tissue
capsule. It consists of helium; the triad of portal vein, hepatic vessels. These
elements branch repeatedly to supply more than one million basic structural units;
the hepatic lobules. Each lobule is formed of hepatocytes arranged around the
central vein; the sinusoids and kuffer cells.
The histopathological changes are presented in plate IX , Fig No. 1
shows T.S. of liver of control rat indicating hepatocytes, central vein, Sinusoids
and Kuffer cells.
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Fig. No. 2 and 3 of Plate IX shows ghost of anuclear cells, hepatocyte
with eosinophilic changes along with sinusoidal cells after 8 hours exposure to
foundry environment.
Fig. No. 4, 5 and 6 shows multinucleated giant cells, polyploidy in
hepatocytes, ghost of a nuclear cells, eosinophilic fluid accumulation and
necrotic cells after 16 hours exposure in foundry environment.
d) Histopathology of kidney:
The kidney is an organ of homeostasis of the internal environment as well as
organ of excretion in higher vertebrates. Kidney cleans the blood plasma of
unwanted substances as it passes through the kidney. Kidney excretes many toxic
metabolic waste products, particularly the nitrogenous molecules, such as urea,
uric acid, certainine compounds that can be conveniently be excreted dissolved in
water. In addition many other ions accumulated in the body in excess quantities
are also removed by kidney. These functions of kidney are impaired by renal
diseases or by adversity of morbid conditions, primarily affecting other tissues and
systems, which include circulatory failure, acid base balance of the organism,
change in the volume of the extra cellular fluid. Kidney deficiency, diseases of the
adrenals, parathyroid gland and other endocrine organs, general metabolic
changes and soon. Various environmental stress factors, toxins affect the normal
functioning of the kidney and produce histophysiological and histopathological
alterations in kidney.
Internally kidney consists of outer cortex and inner medulla zone. The
basic structural and functional unit of kidney is nephron. The kidney of rat consists
of about 30,000 nephrons. Each rephron consist of Malpighian corpuscle formed
of glomerulus and Bowman’s capsule and brings about ultra filtration of blood. The
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renal tubule consists of a simple epithelium that varies from squamous to cuboidal
to columnar. The cells of proximal convoluted tubule (PCT) have elaborate basal
interdigitations and apical microvilli as well as highly developed lysosomal
apparatus involved in the intracellular degradation, of absorbed proteins. PCT
reabsorbs approximately 80% of all proteins, amino acids, glucose, water and
most ions and electrolytes from tubular filtrate. The distal convoluted tubule (DCT)
has fewer microvilli and less elaborate basal labyrinth than PCT, consistent with its
role in hyperosmotic absorption. It has lower ion permeability, loop of Henley
consisting ascending and descending limbs, which are lined by simple squamous
cells with few organelles. The descending limb is permeable to sodium and water,
while ascending limb is not. Sodium pumped out of ascending limb increases the
concentration with interstitial spaces and dilute urine. The loop of Henley functions
to create a linear osmotic gradient in the interstitial space by counter current
multiplication. The collecting duct has an important role in production of
concentrated urine by reabsorption of water under influence of ADH. These normal
functions and structure of nephron can be affected by various kinds of stresses
and toxins, leading to different abnormalities.
In present study following histological alterations were observed in T.S of
kidney of experimental rat (Rattus norvegicus) exposed to foundry environment.
The alterations in the histology of kidney depicted in Plate No. X. The T.S.
of kidney of control rat shows renal tubules normal glomerulus and Bowman’s
space.
Fig. No. 5 and 6 shows accumulation of edematous fluid in medulla region,
and swelling and flattening of renal tubules after 16 hours exposure to foundry
environment.
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Fig No. 7 and 8 shows shrunken glomerulus after 24 hours exposure to
foundry environment.
e) Histopathology of Adrenal Gland:
Pair of adrenal glands located reteroperitoneally and on the superomedial
aspect of the front of kidney. It is composed of morphologically, histologically,
chemically and functionally of two different parts, the adrenal medulla and the
adrenal cortex. The adrenal medulla functionally related to secretion of the
hormones epinephrin and norephinephrin in response to sympathetic stimulation.
The norepinephrin causes constriction of essentially all the blood vessels of the
body. It causes increased activity of heart, inhibition of gastro intestinal tract and
so on. Epinephrin causes almost the same effects as those caused by
norepinephrin, but it has greater effect on cardiac activity, it causes weak
constriction of blood vessels. The metabolic rate of every cell in the body
increased by these hormones especially by epinephrin.
The adrenal cortex secrets entirely different group of hormones called as
corticosteroids. Physiologically most important adrenal cortical hormones can be
divided into 3 groups according to their biological activity, the mineralocorticoids,
acting predominantly on sodium and potassium balance, the glucocorticoids
affecting carbohydrate and protein metabolism and adrenal androgens, which
exhibit approximately the same effects in the body as the testosterone.
Adrenal gland is called as stress gland and stress increases the
organism’s requirement for cortisol. Cortisol secretion often increases growth in
stressful situations this is significant benefit to the animal as they have life saving
role.
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Histologically adrenal gland composed of two distinct parts the adrenal
cortex and the adrenal medulla. The adrenal cortex is composed of three
concentric zones. The outer thin zona glomerulosa, consist of group of small
columnar closely packed epitheloidal cells secreting aldosterone. The middle
largest cortical zone, the zona fasciculata, consists of larger polyhedral cells,
containing two nuclei and large number of lipid droplets, in their cytoplasm.
These cells secrets cortisole and glucocorticoids and small amount of androgen.
The zona reticularis, the deep layer consisting of and anatomizing network of
polygonal epitheloid cells, secreting cortisole, glucocorticoids and adrenal
androgens.
The cells of adrenal medulla are modified post ganglionic cells of
sympathetic nervous system, called chromaffin cells. These cells secrets
epinephrin and nor-epinephrin. Various types of stresses can affect structure and
secretary activity of adrenal gland cells. In present study following histological
changes were observed in the adrenal gland of experimental rat (Rattus
norvegicus) exposed to the foundry environment. These histological changes in
adrenal gland depicted in plate XI. The T.S. of adrenal gland of control rat show
in Fig. No. 1 and 5, which shows normal histological elements of gland such as
zona glomerulosa, zona fasciculata, zona reticularis and adrenal medulla.
Following histological alterations were observed in the adrenal gland of
animals exposed to foundry environment as compared to control animal.
Fig. No. 2 of plate XI of T.S. of Adrenal gland of experimental rat shows
hyperplasia in Zona fasciculata. Fig. No. 3 shows vacuolated cytoplasm in some
of zona fasciculata layer. Fig. No. 4 Shows hypertrophy and vacuolated
cytoplasm in Zona fasciculata as well as lesions in the cells.
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Fig. No. 6 shows changes in adrenal medulla of experimental rat, it shows
granulated cytoplasm and enlarged chromaffin cells. Fig. No. 7 shows localized
hemorrhage in adrenal medulla and Fig No.8 shows on enlargement in
chromaffin cells of medulla.
9. Hematology and Behavior of PMNs:
Erythrocytes, leucocytes and platelets forms the essential cellular
components of the blood. The rates at which these cells are produced are
regulated to match the rates at which they leave the circulation. The
concentration of each cell type is maintained in the blood within well- defined
limits, unless the balance between production and elimination is disturbed by
pathological processes. One of the best and most important procedures in any
hematological evaluation is a careful examination of the formed elements of the
blood. This assessment includes quantification of the concentration of each
cellular element and a careful microscopic examination of the cellular
morphology. The majority of hematologic disorders can be defined by specific
abnormalities in these values; in other pathologic states the blood contains
valuable diagnostic information.
The red cells are most numerous cells, they contain hemoglobin, an iron-
protein complex; these molecules serve as the major carriers of oxygen and
carbon dioxide. The leukocytes are heterogeneous group of nucleated cells
whose major function is to protect the host from the external environment.
Platelets are cytoplasmic fragments which are of importance in homeostasis and
other functions.
Hematological profile of control rats and experimental rats exposed to
foundry environment in different sections, are expressed in Table No. 9 to 13
83
and Plate XII shows blood smear of control rat and experimental rat exposed to
foundry environment. The experimental animals exhibited significant alterations
in hematological profile. These results are as follows:
a. Hemoglobin Level:
The mean hemoglobin concentration in blood of control group of rat was
observed as 9.7 gms/ 100ml. while it shows changes in different sections of
foundry according to exposure period. In S1 (Sand Plant) hemoglobin
concentration in blood shows steady elevation. After 8 hours exposure it was
recorded as 16.3 gms / 100ml, after 16 hours exposure it was recorded as 12.8
gms/100ml and after 24 hours exposure it was found to be 10.6 gm/ 100 ml.
Over all observations up to 24 hours exposure in S1, it was clear that the
hemoglobin concentration increased as compared to control. In the initial
exposure it was maximum up to 16.3 gms/ 100 ml and decreased after 24 hours
i.e. 10.6 gms/ 100 ml. Fig. No. 4 exhibits pattern of hemoglobin level in control
and experimental rats on exposure to different sections of foundry.
In S2 (Fettling Section) hemoglobin concentration in blood shows steady
elevation. After 8 hours exposure it was recorded as 15.4 gms/ 100 ml, after 16
hours exposure it was recorded as 12.6 gms/ 100ml. And after 24 hours
exposure it was found to be 13.4 gms/ 100ml. Over all observations up to 24
hours exposure in S2, it was clear that the hemoglobin concentration is increased
as compared to control.
In S3 (Molding Section) hemoglobin concentration shows steady
elevation, after 8 hours exposure it was recorded as 15.0 gms/100 ml after 16
hours exposure it was recorded as 14.2 gms/ 100ml and 24 hours exposure it
was found to be 13.7 gms/ 100ml. Over all observations up to 24 hours exposure
84
in S3, it was clear that the hemoglobin concentration increased as compared to
control.
In S4 (Furnace Section) hemoglobin concentration shows steady
elevation, after 8 hours exposure it was recorded as 15.6 gms/ 100ml after 16
hours exposure it was recorded as 12.8 gms/100ml and after 24 hours exposure
it was found to be 9.1 overall observations up to 24 hours exposure in S4 section
it was clear that the hemoglobin concentration increased as compared to control
up to 16 hours exposure and after 24 hours it was decreased than control
animal.
In S5 (Core Shop) hemoglobin concentration show steady elevation but
after 24 hours decrease in level of hemoglobin than control animals. After 8
hours exposure hemoglobin level was recorded as 15.1 gms/100ml after 16
hours exposure it was recorded as 14.4 gms/ 100 ml. It was clear that the
hemoglobin concentration increased up to 16 hours exposure but after 24 hours
it starts decreasing as compared to control.
b. Total RBCs Count:
It has been observed that total erythrocyte count in control group of
animal was 4.74 million / mm3 of blood, while it shows changes in different
sections of foundry according to exposure period. In S1(Sand Plant) red cell
count shows steady elevation. After 8 hours exposure it was recorded as 9.30
million/ mm3, after 16 hours exposure it was recorded as 8.60 million/ mm3 and
after 24 hours exposure it was found to be 5.35 million/mm3 overall observation
up to 24 hours exposure in S1, it was clear that the red cell count increased as
compared to control.
85
In the initial exposure it was maximum up to 9.30 million/ mm3 and shows
steady decrease after 24 hours i.e. 5.35 million/mm3. Fig. No.5 exhibits pattern
of red cell count in control and experimental rat on exposure to different sections
of foundry.
In S2 (Fettling Section) red cell count shows steady increase. After 8
hours exposure it was recorded as 7. 86 million/ mm3, after 16 hours exposure it
was recorded as 7.60 million/ mm3 and after 24 hours exposure in S2 it was clear
that the red cell count increased as compared to control.
In S3 (Moulding Section) red cell count shows steady increase. After 8
hours exposure it was recorded as 9.03 million/ mm3 after 16 hours exposure it
was recorded as 8.20 million/ mm3 and after 24 hours exposure it was found to
be 7.38 million/ mm3. Overall observations up to 24 hours exposure in S3, it was
clear that the red cell count increased as compared to control
In s4 (Furnace Section) red cell count shows steady elevation but after 24
hours decrease in red cell count as compared to control animal. After 8 hours
exposure red cell count was recorded as 9.05 million/ mm3, after 16 hours
exposure it was recorded as 7.35 million/ mm3 over all observations up to 24
hours exposure in S4 section, it was clear that red cell count increases up to 16
hours exposure but after 24 hours it starts decreasing as compared to control
animal.
In S5 (Core Shop) red cell count shows steady elevation but after 24
hours decrease in red cell count as compared to control animal. After 8 hours
exposure red cell count was recorded as 9.25 million/ mm3, overall observations
up to 24 hours exposure in S5 section, it was clear that red cell count increases
86
up to 16 hours exposure but after 24 hours it starts decreasing as compared to
control animal.
The microscopic observation of peripheral smear of RBCs exhibit that, in
control group of rat the RBCs are normocytic, normochromic while in
experimental groups of rat the RBCs observed are microcytic, hypochromic
(pale) on 24 hour exposure Plate XI.
C. Total Platelet Count:
The total platelet count in control group of rat is 11,21,000 lakhs/mm3 of
blood, while it shows changes in different sections of foundry according to
exposure period Fig. No.6. In S1 (Sand Plant) Platelets shows steady decrease.
After 8 hours exposure it was recorded as 9,27000 lakhs/mm3, after 16 hours
exposure it was recorded as 7,25,000 lakhs/mm3 and after 24 hours exposure it
was found to be 6,84,000 lakhs/mm3. Overall observation up to 24 hours
exposure in S1 it was clear that the platelet count decreased as compared to
control.
In S2 (Fettling shop) Platelet count also shows steady decrease. After 8
hours exposure it was recorded as 11,18000 lakhs/mm3, after 16 hours exposure
it was recorded as 10,80,000 lakhs/mm3 and after 24 hours exposure it was
found to be 9,40,6000 lakhs/mm3, overall observations up to 24 hours exposure
in S2 it become clear that the platelet count decreased as compared to control.
In S3 (Moulding section) Platelet count shows steady decrease. After 8
hours exposure it was recorded as 8,92,000 lakhs/mm3, after 16 hours exposure
it was recorded as 8,85,000 lakhs/mm3 and after 24 hours exposure it was found
87
to be 8, 57,000 lakhs/mm3. Overall observations up to 24 hours exposure in S3
section, it was clear that the platelets count decreased as compared to control.
In S4(Furnace Section) platelet count also shows decrease. After 8 hours
exposure it was recorded as 9,36,000 lakhs/mm3, after 16 hours exposure it was
recorded as 7,35,000 lakhs/mm3, after 24 hours exposure it was found to be
8,97,000 lakhs/mm3. Overall observations up to 24 hours exposure in section, it
was clear that the platelet count decreased as compared to control. As
compared to platelets count of 24 hours exposure, count was increased than 16
hours exposure, but was less than control.
In S5 (Core Shop) platelet count also shows steady decrease. After 8
hours exposure it was recorded as 8,01,000 lakhs/mm3, after 16 hours exposure
it was recorded as 6,13,000 lakhs/mm3, and after 24 hours exposure it was
found to be 4,61,000 lakhs/mm3. Overall observations up to 24 hours exposure
in S5 Section, it was clear that the platelet count decreased as compared to
control animal. Fig. No. 6.
d. Total WBC count:
The total white blood cell count in control group of rat was 2800/mm3 of
blood, while it shows changes in different sections of foundry according to
exposure period. Fig. No. 7and Shows pattern of total WBCs in control and
experimental rat on exposure to different sections of foundry.
In S1 (Sand Plant) total white blood cell count after 8 hours exposure
period it was recorded as 1100 /mm3, After 16 hours exposure it shows sudden
increase up to 3300 /mm3 and after 24 hours exposure it was again decreased
when compared to control animal.
88
In S2 (Fettling section) total white blood cell count after 8 hours exposure
period it was recorded as 4900 /mm3, after 16 hours exposure it showed
decrease up to 3700 /mm3 and after 24 hours exposure it was 2600 /mm3. As
compare to control, values of WBCS after 8 hours and 16 hours were higher
than control.
In S3 (Molding section) total white blood cell count after 8 hours exposure
period it was recorded as 1800 /mm3, after 16 hours exposure it showed
increase up to 2500 /mm3, and after 24 hours exposure it was again increased
up to 4600 /mm3. As compared to control values of WBCs after 24 hours
exposure were higher.
In S4 (Furnace Section) total white blood cell count after 8 hours
exposure period it was recorded as 3600 /mm3, after 16 hours exposure it was
showed decrease up to 3200 /mm3 and after 24 hours exposure it was again
decreased up to 3100 /mm3. So it this section it showed decreasing trend i.e. in
8 hour exposure values of WBCs are higher than control.
In S5 (Core shop) total white blood cell count after 8 hours exposure it
was recorded as 2700 /mm3, after 16 hours exposure it was found to be 4800
/mm3, and after 24 hours again decreased up to 2500 /mm3. As compared to
control, values of WBCs after 16 hours exposure were quite higher. The values
of WBCs in 8 hours exposure and 24 hours exposure were decreased as
compared to control.
e. Differential WBCs Count:
Table No. 9 to 13 (8) shows observations of differential count of white
blood cells in smear of control and experimental group of rats of different
89
sections of foundry. It has been observed that, the per cent neutrophils in control
group of rat were 46%.
In S1(Sand Plant) percent neutrophil after 8 hours exposure was
recorded as 23%, after 16 hours exposure it was found to be 31% and after 24
hours 42%. As compared to control it has been observed that neutrophil number
in blood smear of experimental rat was decreased. But as exposure period
increased values of neutrophils were elevated. Fig. No. 8 exhibits pattern of
neutrophil per cent in control and experimental rat of S1 section.
In S2 (Fettling Section) percent neutrophil after 8 hours exposure it was
recorded that neutrophil number in blood smear of experimental rat after 8 hours
and 16 hour exposure was found to be decreased but after 24 hours of exposure
thus values of neutrophils were increased. Fig. No. 9 shows pattern of neutrophil
per cent in control and experimental rat of S2 Section.
In S3 (Molding Section) percent neutrophil after 8 hours exposure was
found to be 60% and after 16 hours exposure it was recorded as 55% and after
24 hours it was 60%. As Compared to control it has been observed that
neutrophil number in blood smear of experimental rat was found to be increased.
Fig. No. 10 depicts pattern of neutrophil percent in control and experimental rat
of S3 Section.
In S4 (Furnace Section) Per cent neutrophil after 8 hours exposure was
found to be 50% and after 16 hours exposure it was recorded as 42% and after
24 hours it was 50%. As compared to control it has been observed that
neutrophil number in blood smear of experimental rat was increased, except in
16 hours exposure period per cent neutrophil Values were decreased than
90
control animal. Fig. No. 11 depicts pattern of neutrophil per cent in control and
experimental rat of S4 Section.
In S5 (Core shop) per cent neutrophil after 8 hours exposure was found to
be 40 % and after 16 hours exposure it was recorded as 44% and after 24 hours
it was 48%. As compared to control it has been observed that neutrophil number
in blood smear of experimental rat was decreased, except in 24 hours exposure
period. Percent neutrophil values were decreased than control animal. Fig. No.
12 depicts pattern of neutrophil per cent in control and experimental rat of S5
Section.
The per cent eosinophil count in control group of rat was 2%. In S1 (Sand
Plant) Per cent eosinophil after 8 hours exposure was recorded as 1%, after 16
hours exposure it was found to be 8% and after 24 hours 0.3%. As compare to
control it has been observed that eosinophil number in blood smear of
experimental rat was increased except in 8 hours exposure the values remain
lower than control. Fig. No.13 depicts pattern of per cent eosinophils in control
and experimental rat of S1 Section.
In S2 (Fettling section) percent eosinophil after 8 hours exposure was
recorded as 1%, after 16 hours exposure it was found to be 1% and after 24
hours 4%. As compare to control values of eosinophil per cent remain constant
in 8 hours and 16 hours exposed animals but after 24 hours the values are
elevated in S2 Section. Fig No. 14 exhibits pattern elevated of S2 Section.
In S3 (Molding Section) percent eosinophil after 8 hours exposure was
recorded as 15 %, after 16 hours 2% and after 24 hours it was found to be 4%.
As compare to control values of eosinophil percent were elevated in 8 hours and
24 hours exposure, but in 16 hours exposures percent eosinophil values remain
91
constant to that of control. Fig No.15 depicts pattern of per cent eosinophil in
control and experimental rat constant of S3 section.
In S4 (Furnace Section) per cent eosinophil after 8 hours exposure was
recorded as 9% after 16 hours 4% and after 24 hours it was found to be 3%. As
compare to control values of percent eosinophil were elevated. In 8 hours
exposure values of eosinophil per cent was higher than 16 hours and 24 hours
exposure Fig. No. 16 exhibits pattern of per cent eosinophil in control and
experimental rat of s4 Section.
In S5 (Core Shop) percent eosinophil after 8 hours exposure was
recorded as 4% after 6̀ hours 8% and after 24 hours it was found to be 2% As
compare to control values of per cent eosinophil were elevated. In 16 hours
exposure values of eosinophil percent were higher than 8 hours and 24 hours
exposure. Fig. No. 17 depicts pattern of eosinophil per cent in control and
experimental rat of S5 Section.
The percent lymphocytes count in blood of control group of rat was 50%.
In S1 (Sand Plant) percent lymphocyte after 8 hour exposure was recorded as
75%, after 16 hours exposure it was found to be 59% and after 24 hours 55%.
As compared to control it has been observed that lymphocyte number in blood
smear of experimental rat was elevated Fig. No. 18 depicts pattern of
lymphocyte per cent in control and experimental rat of S1 Section.
The percent lymphocyte in S2 (Fettling Section) after 8 hours exposure
was recorded as 72%, after 16 hours exposure it was found to be 52% and after
24 hours 45 %. As Compared to control it has been observed that lymphocyte
number in blood smear of experimental rat was elevated except in 24 hours
exposure values of percent lymphocytes was decreased than control Fig. No.19
92
depicts pattern of lymphocyte per cent in control and experimental rat of S2
Section.
In S3 (molding section) per cent lymphocyte after 8 hour exposure was
recorded as 22%, after 16 hours exposure it was found to be 30 % and after 24
hours 35 %. As compared to control it has been observed that lymphocyte
number is blood smear of experimental rat was decreased. Fig. No. 20 depicts
pattern of lymphocyte per cent in control and experimental rat of S3 Section.
The percent lymphocyte in S4 (Furnace Section), after 8 hours exposure
was recorded as 58%, after 16 hours exposure it was found to be 42% and after
24 hours 44%. As compared to control it has been observed that lymphocyte
number in blood smear of experimental rat was decreased except in 8 hours
exposure period, it was found to be increased than control Fig. No. 21 shows
pattern of lymphocyte per cent in control and experimental rat of S4 section.
In S5 (Core shop) per cent lymphocyte after 8 hours exposure was 52%,
after 16 hours exposure it was recorded as 47% and after24 hours 45%.As
compared to control it has been observed that lymphocyte number in blood
smear of experimental rat was decreased except in 8 hours exposure period. It
was found to be slightly increased than control Fig. No. 22 shows pattern of
lymphocyte percent in control and experimental rat of S5 Section.
The per cent monocytes observed in control group of rat was 2%. In
s1(sand plant) per cent monocytes after 8 hours exposure was recorded as 1 %,
after 16 hours exposure it was found to be 2% and after 24 hours exposure no
any monocytes found in the blood smear. As compare to control it has been
observed that monocytes number in blood smear of experimental rat was
decreased. Except in 16 hours exposure monocytes percent remain equal to
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control. Fig. No.23 shows pattern of monocytes per cent in control and
experimental rat of S1 section.
In S2 (Fettling section) per cent monocytes after 8 hours exposure was
recorded as 0%, after 16 hours exposure it was found to be 3%, and after 24
hours exposure it was observed 1%. As compare to control it has been observed
that monocyte number in blood smear of experimental rat was decreased except
in 16 hours exposure, monocyte per cent remain elevated than control. Fig. No.
24 shows pattern of monocyte per cent in control and experimental rat of S2
Section.
In S3 (Moulding section) per cent monocytes after 8 hours exposure was
recorded as 3 %, after 16 hours exposure again 3% and after 24 hours exposure
it was observed 1%. As compare to control it has been observed that monocytes
number in blood and smear of experimental rat was increased except in 24
hours exposure, monocytes percent remain decreased than control Fig. No. 25
shows pattern of monocytes per cent in control and experimental rat of S3
Section.
In S4 (Furnace Section) percent monocytes after 8 hours exposure was
recorded as 4%, after 16 hours exposure 4% and after 24 hours exposure it was
observed 3%. As compare to control it has been observed that monocytes
number in blood smear of experimental rat was increased after three types of
exposure periods Fig. No. 26 shows pattern of monocytes per cent in control and
experimental rat of S4 section.
In S5 (Core Shop) percent monocytes after 8 hours exposure was
recorded as 4%, after 16 hours exposure 1% and after 24 hours exposure it was
observed 5%. As compare to control it has been observed that monocytes
94
number in blood smear of experimental rat was elevated except in 16 hours
exposure it fall down to 1% Fig No.27 shows pattern of monocytes per cent in
control and experimental rat of S5 Section.
Overall scenario of blood of rats exposed to different sections of foundry
environment shows that, platelets were significantly decreased except in S3
(Molding Section) after 16 hours exposure they showed
increase. In all section of foundry WBCs showed varied pattern in S2 and S4
initially WBCs were increased, but later on it showed decrease after 16 hours
exposure. In S1, S3, and S5 WBCs showed decrease in number up to 16 hours
they were increased in number. In S3 section after 16 hours exposure WBCs
showed gradual increase in number. RBCs become pale stained with
Leishman’s stain. Microscopic observation of polymorphonuclear leukocytes
reveals that, the shape of multilobed nucleus changes to circular ring like. (Fig.
3, 5 and 6 of Plate XII)
f. Behavior of PMNs:
The polymorphonuclear leukocytes (PMNs) play an important role in
defense actions of body, In present study, it has been observed that, the total
number of leukocytes in the blood circulation of control rat was 2800/mm3 of
blood, this number showed variations in S2 and S4 Sections initially leukocytes
were increased, but showed decrease after 16 hours of exposure. In S1, S3 and
S5 sections leukocytes showed decrease in number up to 8 hours of exposure
but after that number increased. In S3 section there was gradual increase of
leukocytes.
95
The per cent neutrophil values in control rat were 46% but in
experimental rat values show variations in different sections. In S1 values were
decreased. In S2 values of per cent neutrophil showed decrease but in 24 hours
exposures showed increase. In S3 values were increased, in S4 values are
slightly elevated and S5 values are slightly decreased except 24 hours exposure
period.
The movement of leukocytes from the general circulation into the tissue
is a normal process that provides the lung tissue with macrophages required to
clear foreign material and the lymphocytes need to maintain immune
surveillance. The PMNs are unique in that they remain with the vascular space
unless. They are required to migrate into inflammatory site. The significant
decrease in the percent PMNs values have been observed with simultaneous
appearance of PMNs in the brancheoalveolar lavage (Fig No. 3 to 6 Plate VI).
10. Liver Functions Tests:
Whenever dysfunction occurs in a tissue it has the origin in biochemical
derangements at the sub cellular level. Recourse in made to appropriate function
test, designed to explain subtle effects. The biochemical abnormality, revealed
by such tests, may become apparent before the onset or morphological damage
and precede the development of degenerative disease.
The prevalence of hepatotoxic effects, together with the multitude of
metabolic activities in which liver is involved, has greatly promoted the liver
function tests. Toxic damage to the liver causes three types of functional
disturbances:
96
I. Metabolic impairment
II. Changes in secretory or excretory efficiency and
III. Diminished ability for detoxification.
Liver is unique important and largest organ in abdominal cavity which
perform various types of functions such as synthesis (albumin, clotting factors,
transport proteins i.e. cholesterol, steroid hormones and bilirubin), detoxification
(Xenobiotics), excretion (formation of bile) and digestion (role of bile salts in
triglyceride absorption).
Any liver injury without any histological change and any organ
dysfunction can be conformed by serum biochemical test. It has been
recommended that, the “Liver Function Tests” reflects physiological functions of
the liver.
Liver function test most often used to determine, the presence of liver
disease, type of liver disease and the extent and progression of liver disease. It
has been carried out to observe the excretion by the liver (Bile pigment Bilirubin),
evaluation of synthesis in liver (serum proteins) and evaluation of enzyme
activity specifically like alkaline phosphates.
a. Serum Bilirubin (Bile Pigment):
The level of serum bilirubin concentration depends up on rate of removal
of bilirubin from destruction of hemoglobin. In the blood bilirubin is present as
“indirect” reacting bilirubin which is not water soluble and “direct” reacting
etherified bilirubin which is water soluble. The sum total of direct and indirect
bilirubin regarded as total bilirubin in blood.
97
It has been observed that, in control group of rat total bilirubin level was
1.2 gms/100ml while it showed changes in different sections of foundry
according to exposure period. It was shown in table No. 14 to 18 and Fig. No. 28
to 32.
In S1 (Sand Plant) total bilirubin level after 8 hours exposure period was
recorded as 0.6 gms/100ml. After 16 hours exposure it showed slight elevation
up to 0.8 gms/100ml and after 24 hours exposure it was again elevated up to 1.0
gm/100ml. As compared to control it has been observed that values of bilirubin
were decreased. Fig. No.28 depicts changes in bilirubin level in S1.
In S2 (Fettling Section) total bilirubin level after 8 hours exposure period
was recorded as 0.7gms/100ml. After 16 hours exposure 0.8gms/100ml and
after 24 hours exposure. It was elevated up to 1.0 gm/100ml. As compared to
control it has been observed that values of bilirubin were decreased. Fig. No.29
exhibits changes in bilirubin level in S2.
In S3 (Molding Section) total bilirubin level after 8 hours exposure period
was recorded as 0.3 gms/100ml. after 16 hours exposure 1.0 gms/100ml and
after 24 hours exposure it was recorded as 0.9 gms/100ml. as compared to
control it has been observed that values of bilirubin were decreased Fig. No. 30
depicts changes in bilirubin level in S3.
In S4 (Furnace section) total bilirubin level after 8 hours exposure was
found to be 0.2 gms/100ml. after 16 hours exposure and 24 hours exposure it
was recorded as similar 0.8gms/100ml. as compared to control it has been
observed that values of bilirubin were decreased. Fig. No.31 exhibits changes in
bilirubin level in S4.
98
In S5 (Core Shop) total bilirubin level after 8 hours exposure was found to
be 0.1 gm/100 ml after 16 hours exposure 0.6gms/100ml and 24 hours exposure
it was recorded as 1.0 gm/100ml. as compared to control it has been observed
that values of bilirubin were decreased. Fig. No. 32 exhibits changes in bilirubin
level in S5.
Direct bilirubin level in control group of rat was observed as
0.4gms/100ml. It shows changes in different sections of foundry according to
exposure period. It was shown in Table No. 14 to 18.
In S1 (Sand Plant) direct bilirubin level after 8 hours exposure was 0.4
gms/100ml. after 16 hours exposure 0.2 gms/100ml and after 24 hours exposure
it was recorded as 0.6 gms/100ml. As compared to control it has been observed
that values of direct bilirubin were decreased.
In S2 (Fettling Section) direct bilirubin level after 8 hours exposure was
0.9 gms/100ml. after 16 hours exposure 0.2 gms/100ml and after 24 hours
exposure it was recorded as 0.6 gms/100ml. As compared to control in 8 hours
and 24 hours of exposed animals shows elevated values of direct bilirubin.
In S3 (Moulding Section) direct bilirubin level after 8 hours exposure was
0.1 gms/100ml. after 16 hours exposure 0.2 gms/100ml and after 24 hours
exposure it was recorded as 0.4 gms/100ml. As compared to control it has been
observed that values of direct bilirubin were decreased.
In S4 (Furnace Section) direct bilirubin level after 8 hours exposure was
0.1 gms/100ml. After 16 hours exposure 0.2 gms/ 100ml and after 24 hours
exposure it was recorded as 0.3 gms/100ml. As compared to control it has been
observed that values of direct bilirubin were decreased.
99
In S5 (Core Shop) direct bilirubin level after 8 hours exposure was 0.1
gms/ 100ml. After 16 hours exposure 0.1 gms/100ml and after 24 hours
exposure it was recorded as 0.5 gms/100ml. which shows slight elevation in
level of bilirubin. As compared to control it has been observed that values of
direct bilirubin were decreased.
Indirect bilirubin level in control group of rat was observed as 0.8
gms/100ml. It shows changes in different sections of foundry according to
exposure period. It was shown in Table No. 14 to18.
In S1 (Sand Plant) indirect bilirubin level after 8 hours exposure was 0.2
gms/100ml and after 24 hours exposure it was recorded as 0.4 gms/100ml. As
compared to control it has been observed that values of indirect bilirubin were
decreased.
In S2 (Fettling Section) indirect bilirubin level after 8 hours exposure was
0.4 gms/100ml. After 16 hours exposure 0.6 gms/100ml and after 24 hours
exposure it was recorded as 0.4 gms/100ml. As compared to control it has been
observed that values of indirect bilirubin were decreased.
In S3 (Moulding Section) indirect bilirubin level after 8 hours exposure
was 0.2 gms/100ml. After 16 hours exposure 0.1 gms/100ml and after 24 hours
exposure it was recorded as 0.5 gms/100ml. As compared to control it has been
observed that values of indirect bilirubin were decreased.
In S4 (Furnace Section) indirect bilirubin level after 8 hours exposure was
0.1gms/100ml.after 16 hours it was 0.6 gms/100ml and after 24 hours exposure
it was recorded as 0.5 gms/100ml. When compared to control it has been
observed that values of indirect bilirubin were decreased.
100
In S5 (core shop) indirect bilirubin lever after 8 hours exposure was nil.
After 16 hours it was 0.5gms/100ml and after 24 hours exposure it was noted as
0.5 gms/100ml. When we compared to control it has been observed that values
of indirect bilirubin were decreased.
11. Serum Proteins:
Serum proteins are synthesized in liver, serum proteins shows alterations
in level on exposure to occupational environmental stress factors. The changes
in the level of serum albumin and globulin provide valuable indices regarding
physiological status of liver. In our study the level of total serum proteins albumin
and globulin was measured by biochemical methods.
The mean values of total serum proteins observed in control group of rat
are 8.0 gm/100ml while in experimental animal on exposure to different sections
of foundry according to different exposure periods shows alterations as shown in
Table No.14 to 18(2) and Fig No.33 to 37.
In S1 (Sand Plant) total serum proteins level after 8 hours exposure
period was recorded as 6.9 gms/100ml. after 16 hours exposure 10.2 gms/100ml
and after 24 hours exposure it was recorded as 8.0 gms/100ml. as compared to
control it has been observed that values of total serum proteins increased after
16 hours exposure and decreased after 8 hour exposure while after 24 hours
exposure it was similar to control. Fig No. 33 depicts changes in total serum
proteins in S1 Section.
In S2 (Fettling Section) total serum proteins level after 8 hours exposure
period was recorded as 7.6 gms/100ml. After 16 hours exposure 9.9 gms/100ml
and after 24 hours exposure it was recorded as 8.0 gms/100ml. As compared to
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control it has been observed that values of total serum proteins elevated after 16
hours exposure and decreased after 8 hours exposure, while after 24 hours
exposure. It was similar to control Fig. No.34 exhibits changes in total serum
proteins in S2 section.
In S3 (Molding Section) total serum protein level after 8 hours exposure
period was recorded as 7.3 gms/100ml. After 16 hours exposure 8.9 gms/100ml
and after 24 hours exposure it was recorded as 9.0 gms/100ml. As compared to
control values it has been observed that total serum proteins were increased
after 16 hours and 24 hours exposure and decreased after 8 hours exposure.
Fig. No. 35 shows changes in total serum proteins in S3 section.
In S4 (Furnace section) total serum proteins level after 8 hours exposure
period was 8.0 gms/100ml. After 16 hours exposure 9.5 gms/100ml. after 16
hours exposure 9.5 gms/100ml and after 24 hours exposure it was recorded as
8.5 gms/100ml. As compared to control it has been observed that total serum
proteins were increased after 16 hours and 24 hours exposure and decreased
after 16 hours and 24 hours exposure and decreased after 8 hours exposure.
Fig. No. 36 shows changes in total serum proteins in S4 section.
In S5 (Core Shop) total serum protein level after 8 hours exposure period
was 6.7 gms/100ml. As compared to control it has been observed that total
serum proteins were decreased after 8 hours and 24 hours exposure and
significantly elevated after 16 hours exposure Fig. No. 37 shows changes in total
serum proteins in S5 Section.
The mean values of albumin observed in control group of rat was 5
gms/100ml, while in experimental animal on exposure to different sections of
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foundry according to different exposure periods shows alteration as shown in
Table Nos. 14 to 18(2) and Fig. Nos. 33 to 37.
In S1 (Sand Plant) serum albumin level after 8 hours exposure period
was 4.6 gms/100ml. after 16 hours exposure 4.0 gms/100ml and after 24 hours
exposure it was recorded as 5.4 gms/100ml. As compared to control it has been
observed that values of total serum albumin were decreased after 8 and 16
hours exposure and slightly increased after 24 hours exposure Fig No.33 depicts
changes in total serum albumin levels in S1 section.
In S2 (Fettling Section) serum albumin level after 8 hours exposure period
was recorded as 5.0 gms/100ml. after 16 hours exposure 4.5 gms/100ml and
after 24 hours exposure it was recorded as 5.4 gms/100ml. As compared to
control it has been observed that value of serum albumin 8 hours exposure was
similar to that of control but decreased after 16 hours exposure and increased
after 24 hours exposure Fig No. 34 depicts changes in serum albumin in S2
section.
In S3 (Moulding Section) serum albumin level after 8 hours exposure
period was recorded as 4.4 gms/100ml. after 16 hours exposure 4.9 gms/100ml
and after 24 hours exposure it was recorded as 4.7 gms/100ml. As compared to
control values it has been observed that serum albumin level were depleted in all
exposure periods. Fig. No. 35 shows changes in total serum albumin in S3
Section.
In S4 (Furnace Section) serum albumin after 8 hours exposure period
was 5.0 gms/100ml. after 16 hours exposure 4.8 gms/100ml and after 24 hours
exposure it was recorded as 4.8 gms/100ml. As compared to control it has been
observed that total serum albumin was decreased except in 8 hours exposure
103
values are similar to control. Fig. No. 36 shows changes in total serum albumin
in S4 section.
In S5 (Core Shop) total serum albumin level after 8 hours exposure
period was 4.5 gms/100ml. After 16 hours exposure 5.5 gms/100ml and after 24
hours exposure it was recorded as 4.0 gms/100ml. As compared to control it has
been observed that serum albumin level was depleted in 8 and 24 hours
exposure but elevated after 16 hours exposure. Fig No.37 shows changes in
serum albumin in S5 section.
The mean values of globulin observed in control group of animal are 3.0
gms/100ml. while in experimental animal on exposure to different sections of
foundry according to various exposure periods shows alterations as shown in
Table Nos. 14 to 18(2) and Fig. Nos. 33 to 37.
In S1 (Sand Plant) serum globulin level after 8 hours exposure period was
recorded as 3.0 gms/100ml. after 16 hours exposure 6.2 gms/100ml and after 24
hours exposure it was recorded as 2.6 gms/100ml. As compared to control it has
been observed that values of serum globulin were decreased except in 16 hours
exposure it was found to be elevated than control. Fig. No. 33 depicts changes in
serum globulin level in S1section.
In S2 (Fettling section) serum globulin after 8 hours exposure period was
recorded as 2.6 gms/100ml. After 16 hours exposure 5.4 gms/100ml and after 24
hours exposure it was recorded as 2.6 gms/100ml. As compared to control it has
been observed that values of serum globulin were depleted except in 16 hours
exposure it was found to be elevated than control. Fig No. 34 depicts changes in
serum globulin level in S2 section.
104
In S3 (Molding Section) serum globulin after 8 hours exposure period was
recorded as 2.9gms/100ml. After 16 hours exposure it was recorded 4.3
gms/100ml. As compared to control it has been observed that values of serum
globulin were elevated except in 8 hours exposure it was slightly decreased than
control. Fig No. 35 shows changes in serum globulin levels in S3 section.
In S4 (Furnace Section) Serum globulin level after 8 hours exposure
period was 3.0 gms/100ml. after 16 hours exposure 4.7 gms/100ml and after 24
hours exposure it was recorded as 3.7 gms/100ml. As compared to control it has
been observed that serum globulin level was increased except in 8 hours
exposure it remains equal to control Fig. No. 36 exhibits changes in serum
globulin level in S4 section.
In S5 (Core Shop) Serum globulin level after 8 hours exposure period
was 2.2 gms/100ml. after 16 hours exposure 6.1gms/100ml and after 24 hours
exposure it was recorded as 3.8 gms/100ml. As compared to control it has been
observed that serum globulin level was increased except in 8 hours exposure
period. Fig. No. 37 exhibits changes in serum globulin level in S5 section.
All mean values of total serum protein, albumin and globulin are shown in
Table Nos. 14 to 18(2). The overall observation of Albumin, Globulin ratio
reveals that the globulin levels found to be raised on exposure to different
sections of foundry Fig. No.33 to 37 depicts changes in serum proteins levels in
control and experimental rat of different sections of foundry.
105
12. SERUM ENZYMES
a) Serum Alkaline Phosphatase
The Serum alkaline phosphatase normally present in liver and excreted
through the bile, so the elevation of serum alkaline phosphatase may be
manifestation of retention.
The recognition of serum enzyme increases as a common event in liver
disease, whether infectious, hypoxic or toxic in origin. The particular value of
serum enzyme assay rests upon its capacity to initiate initial cell degeneration
occurring in gross hepatic pathology. The enzymes most frequently employed
are the transaminase, the CKMB, CPK, SGOT and SGPT.
It has been observed that the mean values of alkaline phosphates in
experimental animal on exposure exhibits changes according to exposure period
in different sections of foundry as shown in Table No. 14 to18(3) and Fig. No. 38.
In S1 (Sand Plant) serum alkaline phosphatase level after 8 hours exposure
period was recorded as 222.8 U/L. After 16 hours exposure 1381.8 U/L and after
24 hours exposure it was recorded as 762 U/L. As compared to control it has
been observed that values of serum alkaline phosphates were depleted after 8
hours exposure and elevated after 16 and 24 hours exposure. Fig. No.38
exhibits changes in serum alkaline phosphatase.
In S2 (Fettling Section) serum alkaline phosphatase level after 8 hours
exposure period was recorded as 249.84 U/L. After 16 hours exposure 1032.2
U/L and after 24 hours exposure it was recorded as 740.2 U/L. As compared to
control it has been observed that values of serum alkaline phosphatase were
depleted after 8 hours exposure and elevated after 16 and 24 hours exposure.
106
In S3 (Moulding Section) serum alkaline phosphatase level after 8 hours
exposure period was recorded as 449.0 U/L. After 16 hours exposure 912.3 U/L
and after 24 hours exposure it was recorded as 960.6 U/L. As compared to
control it has been observed that values of serum alkaline phosphatase were
depleted after 8 hours exposure and elevated after 16 and 24 hours exposure.
In S4 (Furnace Section) serum alkaline phosphatase level after 8 hours
exposure period was recorded as 462.0 U/L. After 16 hours exposure 990.4 U/L
and after 24 hours exposure it was recorded as 900 U/L. As compared to control
it has been observed that values of serum alkaline phosphatase were depleted
after 8 hours exposure and elevated after 16 and 24 hours exposure.
In S5 (Core Shop) serum alkaline phosphatase level after 8 hours
exposure period was recorded as 303 U/L. After 16 hours exposure 1057.0 U/L
and after 24 hours exposure it was recorded as 926 U/L. As compared to control
it has been observed that values of serum alkaline phosphatase were decreased
after 8 hours exposure and elevated after 16 and 24 hours exposure.
13. Other Serum Enzymes:
a. Creatine Phosphokinase:
Higher concentration of creatine phosphokinase found in heart muscle,
skeletal Muscle, brain and very negligible activity found in liver, lung kidney and
pancreas. The serum creatine phosphokinase (CPK) level increases in
myocardial infraction and under cardiopulmonary stress. Table Nos. 19 to 21(1)
and Fig. No. 39 shows alterations in creatine phosphokinase of control rat and
experimental rat exposed to different sections of foundry environment.
107
It has been found that the level of CPK in control rat was 1917.0 U/L
while values show alterations according to exposure period in different sections
of foundry.
In S1 (Sand Plant) Serum creatine phosphokinase (CPK) level after 8
hours exposure period was recorded as 696.4 U/L. After 16 hours exposure
period 1619.4 U/L and after 24 hours exposure period it was recorded as 615
U/L. As compared to control it has been observed that value of serum creatine
phosphokinase were declined after 8 hours and 24 hours exposure and elevated
after 16 hours exposure. Fig. No. 39 shows changes in serum CPK.
In S2 (Fettling Section) Serum creatine phosphokinase (CPK) level after 8
hours exposure period was recorded as 2471.0 U/L. After 16 hours exposure
period 1819.5 U/L and after 24 hours exposure period it was recorded as 962
U/L. As compared to control it has been observed that values of serum creatine
phosphokinase were elevated after 8 hours exposure and declined after 16
hours and 24 hours exposure Fig. No. 39 shows changes in serum CPK.
In S3 (Moulding Section) Serum creatine phosphokinase (CPK) level after
8 hours exposure period was recorded as 1818.2 U/L. After 16 hours exposure
period 2224.2 U/L and after 24 hours exposure period it was recorded as 1372.0
U/L. As compared to control it has been observed that value of serum creatine
phosphokinase were elevated after 16 hours exposure and declined after 8
hours and 24 hours exposure.
In S4 (Furnace Section) Serum creatine phosphokinase (CPK) level after
8 hours exposure period was recorded as 1903 U/L. After 16 hours exposure
period 1550 U/L and after 24 hours exposure period it was recorded as 1581
108
U/L. As compared to control it has been observed that value of serum CPK were
declined in 8, 16 and 24 hours exposure.
In S5 (Core Shop) Serum creatine phosphokinase (CPK) level after 8
hours exposure period was recorded as 2031.7 U/L. After 16 hours exposure
period 822.7 U/L and after 24 hours exposure period it was recorded as 1675
U/L. As compared to control it has been observed that value of serum creatine
phosphokinase (CPK) level was elevated after 8 hours exposure and after 16
hours and 24 hours were declined. Fig. No. 39 shows changes in serum creatine
phosphokinase (CPK).
b. Creatine Kinas Muscle and Brain (CKMB):
Creatine Kinase (CK) is dimeric molecule composed of subunits ‘M’
(muscle) and ‘B’ (brain). This is immunologically distinct. The subunits combine
to form (CKMB). The level of CKMB remains increased in cardiovascular
disorder, pulmonary infraction and in convulsive disorders.
It has been observed that the mean values of isoenzyme Creatine Kinase
Muscle and Brain (CKMB) in control group of rat was 967.2 U/L while the values
of CKMB in experimental animal on exposure exhibits changes according to
exposure period in different sections of foundry as shown in Table No. 19 to
21(2) and Fig. No. 40.
In S1 (Sand Plant) CKMB level after 8 hours exposure period was
recorded as 565.8 U/L. After 16 hours exposure period 1210 U/L and after 24
hours exposure period it was recorded as 507.8 U/L. As compared to control it
has been observed that values of CKMB were declined after 8 hours and 16
109
hours of exposure and elevated after 16 hours exposure Fig. No. 40 shows
changes in CKMB.
In S2 (Fettling Section) CKMB level after 8 hours exposure period was
recorded as 1336.0 U/L. After 16 hours exposure period 2797 U/L and after 24
hours exposure period it was recorded as 2952.0 U/L. As compared to control it
has been observed that values of CKMB were elevated according to increase in
exposure period. Fig. No. 40 shows changes in CKMB.
In S3 (Molding Section) CKMB level after 8 hours exposure period 464.9
U/L. After 16 hours exposure period 1720.3 U/L and after 24 hours exposure
period it was recorded as 1581.0 U/L. As compared to control it has been
observed that values of CKMB were elevated after 16 and 24 hours exposure
and declined after 8 hours exposure Fig. No. 40 shows changes in CKMB.
In S4 (Furnace section) CKMB level after 8 hours exposure period was
1637.0 U/L. After 16 hours exposure period 1103.4 U/L and after 24 hours
exposure period it was recorded as 1372.0 U/L. As compared to control it has
been observed that values of CKMB were significantly elevated after each
exposure and Fig. No. 40 shows changes in CKMB.
In S5 (Core Shop) CKMB level after 8 hours exposure period was 1223.0
U/L. After 16 hours exposure period 648.3 U/L and after 24 hours exposure
period it was recorded as 1938 U/L. As compared to control it has been
observed that values of CKMB were elevated after 8 hours and 24 hours
exposure. Fig. No. 40 shows changes in CKMB.
110
C. Serum Glutamate Oxaloacetate Transaminase (SGOT):
Table Nos. 19 to 21 (3) and Fig. No. 41 shows the level of SGOT in
control and experimental rats exposed to different sections of foundry
environment. It has been found that the level of SGOT in control rat was 685
U/L. while these values shows alterations according to exposure period in
different sections of foundry.
In S1 (Sand Plant) SGOT level after 8 hours exposure period was
recorded as 338 U/L. After 16 hours exposure period 465 U/L and after 24 hours
exposure period it was recorded as 477 U/L. As compared to control it has been
observed that values of SGOT were significantly decreased. Fig. No. 41 shows
changes in SGOT.
In S2 (Fettling Section) SGOT value after 8 hours exposure period was
recorded as 362.20 U/L. After 16 hours exposure period it was 551 U/L. As
compared to control it has been observed that values of SGOT were decreased.
In S3 (Moulding Section) SGOT value after 8 hours exposure period was
recorded as 456.0 U/L. After 16 hours exposure period it was 716.0 U/L and
after 24 hours exposure period it was recorded as 533 U/L. As compared to
control it has been observed that values of SGOT were decreased after 8 and 24
hours exposure and elevated after 16 hours exposure.
In S4 (Furnace Section) SGOT values after 8 hours exposure period was
recorded as 356 U/L. After 16 hours exposure period 363.3 U/L and after 24
hours exposure period it was recorded as 533.0 U/L. As compared to control it
has been observed that values of SGOT were significantly decreased in all
cases of exposure period. Fig. No. 41 shows changes in SGOT values.
111
In S5 (Core Shop) SGOT value after 8 hours, exposure period was
recorded as 307 U/L. after 16 hours exposure period 348 U/L and after 24 hours
exposure period it was recorded as 544 U/L. As compared to control it has been
observed that values of SGOT were significantly decreased in all cases of
exposure period. Fig. No. 41 shows changes in SGOT values.
d. Serum Glutamate Pyruvate Transaminase (SGPT):
Table Nos. 19 to 21(4) and Fig.No.42 shows the level of SGPT in control
and experimental rats exposed to different sections of foundry environment. It
has been observed that the level of SGPT in control rat was 76 U/L while these
values shows alterations according to exposure period in different sections of
foundry.
In S1 (Sand Plant) SGPT value after 8 hours exposure period was
recorded as 19.90 U/L. After 16 hours exposure period 187.2 U/L and after 24
hours exposure period it was recorded as 132 U/L. As compared to control it has
been observed that values of SGPT were significantly increased after 16 and 24
hours exposure and decreased after initial 8 hours exposure. Fig. No. 42 shows
changes in SGPT.
In S2 (Fettling Section) SGPT value after 8 hours exposure period was
recorded as 58.30 U/L. After 16 hours exposure period it was 151.0 U/L and
after 24 hours exposure period it was recorded as 144.0 U/L. As compared to
control it has been observed that values of SGPT were almost doubled after 16
and 24 hours exposure and decreased after 8 hours exposure.
In S3 (Moulding Section) SGPT value after 8 hours exposure period was
recorded as 107 U/L. After 16 hours exposure period it was recorded as 140 U/L.
112
As compared to control it has been observed that values of SGPT were elevated
in all exposure periods. Fig. No. 42 shows changes in SGPT.
In S4 (Furnace section) SGPT values after 8 hours exposure period was
recorded as 93.0 U/L. After 16 hours exposure period 132 U/L and after 24 hours
exposure period it was recorded as 140 U/L. As compared to control it has been
observed that values of SGPT were significantly increased as exposure period
increased in all cases. Fig. No. 42 Shows changes in SGPT values.
In S5 (Core shop) SGPT values after 8 hours exposure period was
recorded as 74 U/L. After 16 hours exposure period 100 U/L and after 24 hours
exposure period it was recorded as 186 U/L. As compared to control it has been
observed that values of SGPT were significantly elevated after 16 and 24 hours
exposure and slightly decreased after 8 hours exposure. Fig. No. 42 shows
changes in SGPT values.