OBSERVATION - Shodhgangashodhganga.inflibnet.ac.in/bitstream/10603/43584/13/13_chapter_03.pdf · in...

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59 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 6 th largest producer of castings in the world after U.S, China, Japan, Russia and Germany. India ranks 2 nd 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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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

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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

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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.

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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

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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

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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.

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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

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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

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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

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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

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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

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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.

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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:

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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.

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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.

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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.

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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.

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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

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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.

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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.

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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.

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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.

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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

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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

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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.

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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.

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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.

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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.