1
Monika Rani Saha
Assistant Professor
Department of Pharmacy, University of Rajshahi
ENVIRONMENTAL CHEMISTRY
2
Carbon monoxide
Carbon monoxide: It is an odourless and
colourless gas
It is originated in the incomplete combustion of
carbonaceous materials. It is highly poisonous gas.
Sources:
1. The chief source of CO in atmosphere is
combustion due to the automobile exhausts.
2. When coal, wood and oil are burnt, black smoke is
produced which contain CO.
3.Cigarette smoke also contain CO.
3
Continued
4. Some industrial operation such as electric and blast
furnaces, some petroleum refining operations, gas
manufacturing plants and mines are contributors of
CO to the atmosphere.
Effects:
1. Co has a strong affinity for combining with the
haemoglobin of the blood to form
carboxyhaemoglobin. This reduces the ability of
the haemoglobin to carry oxygen to the body
tissue.
2. CO also affects the CNS. It is also responsible for
heart attacks.
4
Oxides Of NITROGEN
Oxides of nitrogen are the most abandoned
atmospheric contaminant.
Sources:
1. Smoke released by automobile engines contains
oxides of nitrogen.
2. Highest concentration of NO2 in gaseous emission
occurs form industries where nitric acid is produced
or used in chemical reaction.
3. In many chemical industries which manufacture
explosives and nitrogenous fertilizers also produce
oxides of nitrogen.
5
4. Also present in tobacco smoke.
5. Large amount of nitrogen oxides are also emitted
from power plants.
6. When coal, oil and natural gas undergo combustion
at high temperature produce N2 and O2 which upon
combination in atmosphere produce NO and NO2
N2 + O2
110℃
2NO
O2
2NO2
Effects: 1. NO2 is very corrosive and affect skin.
2. NO2 helps in formation of smog which causes
irritation in eye due to the presence of O3.
3. NO2 provides HNO3 by reacting with rainy water
and moisture.
4NO2 + 2H2O + O2  4HNO3
Continued
6
The HNO3 acid then comes down as acid rain or acid
snow. It makes the lakes so acidic that they can no
longer support fish life. The production of agricultural
crops is also reduced.
4. It is estimated that eye and nasal irritation will be
observed after exposure to about 15 ppm of NO2 and
pulmonary discomfort after brief exposure to 25 ppm
of NO2.
Continued
7
Continued
Hydrocarbons
# Chemical compounds which contain, C and H is
called hydrocarbon. It is denoted by CxH2x+2
# Most motor vehicles and engines are powered by
hydrocarbon based fuels such as gasoline and diesel.
# Hydrocarbon pollution results when unburned and
partially burned fuel emitted from the engine as
exhaust and also when fuel evaporates directly into
the atmosphere.
8
Sources:
i. Road mobile sources : bus, truck, car etc.
ii. Non-road mobile sources : train, marine vehicles,
aircraft etc.
iii. Others not mobile sources :
-agricultural sources, -petroleum
-forest fire, -coal
Effects:
Health impact of hydrocarbons:
 Acute respiratory symptoms
 Headaches
 Vomiting
 Brain damage
Continued
9
 Reduced cardiovascular function
 Irritation of eye, nose and throat
 Dizziness
 Coma
 Premature death
 Arrhythmia
 High concentrations have carcinogenic effects on
lungs.
(B) Environmental impact of hydrocarbons
(i) Major components of smog.
(ii) Inhibit plant growth and damage leaf tissues and
death of following plants.
Continued
10
Pesticides: A pesticide is a substance or mixture of
substance-used to kill pest. A pesticide is any substance
intended for preventing, destroying, repelling or
migrating any pest. A pesticide may be a chemical
substance, biological agent (bacteria, virus),
antimicrobial disinfectant or device used against pest.
Pest includes- insects plant pathogens, birds, and
microbes etc.
Source of Pesticides
i. Elemental sulphur
ii. Toxic chemical (arsenic, lead, mercury)
iii. Nicotine sulphate
iv. Organochlorine infectant (DDT)
v. Triazine and others nitrogen base compound
Pesticides
11
 1. Algaecides: The substances which are used for
the control of Algae.
 2. Avicides: The substances which are used for the
control of Birds.
 3. Virucides: The substances which are used for
the control of viruses.
 4. Bactericides: The substances which are used for
the control of bacteria.
 5. Fungicides: The substances which are used for
the control of Fungi.
 6. Herbicides: The substances which are used for
the control of weeds.
 7. Insecticides: The substances which are used for
the control of insects.
Classification of pesticides
12
Effects:
A) Health effect
i) Non-Hodgkin lymphoma is Produced
ii) Leukemia
iii) Prostate cancer
iv) Multiple myeloma and soft tissue sarcoma
B) Acute health problem
i) Abdominal pain
ii) Skin and eye problem
iii) Dizziness
iv) Nausea
v) Vomitting.
Pesticides
13
Cigarattes smoke: The air pollution by cigarattes is 10
times greater than diesel car exhaust cigarattes contain
4000 chemicals in which 48% is carcinogenic.
 Sources:
i. Smoke
ii. Tiny particles (about 4000 chemicals packed
into the cigarattes
iii. Additional dangerous product: CO
 Effects:
 1. Cigarettes smoke contain carcinogenic
ingredient such as arsenic tar and CO which
damages the lungs function.
Cigarettes
14
 2. Nicotine is the additive component contain in
cigaratte smoke is also a potent stimulant. It raises
blood pressure and increases the heart rate.
 3. In regular smoke, nicotine can lead to
cardiovascular complications such as enlarge heart
arrhythmia and coronary artery diseases.
 4. Cigarettes smoke is interfering with the
production of insulin which is responsible for
allowing blood sugar to enter the body cell.
 5. Cigaratte smoke can causes lung cancer
Cigarettes
15
Passive /Involuntary / Second hand smoking:
Breathing other people smoke is called passive /
Involuntary / Second hand smoking.
Effects:
i. Eye irritation
ii. Headaches
iii. Cough
iv. Dizziness
v. Nausea
Those people who regularly inhale other smoke have a 20-
30% greater risk of contracting lung cancer and heart
diseases.
In children Tobacco smoke is especially dangerous for
children. Those who are exposed to basic smoke during
early infancy and childhood has a greater risk of
bronchitis, preumonia and other chest illness.
Cigarettes
16
 Heavy Metal Toxicology is the science of study of
toxic metals and their mode of action.
 These are discharged by industries to air water and
soil. They entered into the human food chain from
the environment. Once they enter our biological
system, they disturb the biochemical processes
leading in some cases to fatal results.
Factors affecting toxicity:
 Route a administration e.g. oral, nasal etc.
 ii. Age
 iii. Sex
 iv. Single or multiple dose
 v. Species of the component.
Heavy Metal Toxicology
17
 Lead (Pb) is heavy, soft, bluish metal and occurs in
nature in the form of ores. Once Pb is mined,
processed and introduced into the environment, it
is a potential problem forever.
 ‘Lead is a highly toxic substance that is harmful
when it enters the body. This situation is called lead
poisoning. Lead poisoning is preventable and is not
contagious.
Sources:
 1. Burning of fuel in vehicle
 2. Industries where lead is extracted.
 3. Lead pipes.
 4. Tinned food.
 5. Decorated candles, coloured photography, hair
drier, paints etc.
Lead poisoning
18
The chemical form of Pb is an important factor
affecting its biological behavior in the body.
1. Lead is a general protoplasmic poison which
accumulates in body and they are slow acting and
stable.
2. Organic lead compounds such as tetraethyl lead
are readily absorbed by the body through the skin or
mucous membranes. This is a serious problem for
occupationally exposed workers whose are involved in
the manufacture of such compounds.
Toxic effect of lead in the body
19
3. Inorganic lead is absorbed primarily through the
gastro-intestinal and respiratory tracts and it is the
main source of lead in the body.
4. It obstructs the utilization of O2 and glucose and
hinders the production of energy.
5. The toxic action of lead in the body is the
enzyme inhibition by the Pb2+ ion. The inhibited
enzyme is necessary for the formation of hemoglobin.
The inhibition is a result of a strong interaction
between Pb2+ and the sulfur groups of some amino
acids of the enzyme.
Continued
20
6. The lead retained in the body from both air and
dietary source accumulates predominantly in the
skeleton . It’s accumulation cause loss of weight,
loss of teeth, constipation etc.
7. An unpleasant aspect of bone accumulated lead
is that it may be remobilized and sent to other parts of
the body long after the initial absorption. This
remobilized can occur during feverish illness as a
result of cortisone treatment and as a result of old age.
Because the determination of lead in bones in difficult,
the concentration of lead in blood or urine is
commonly used as indication of total lead in the body.
Continued
21
1. Since the major source of Pb pollution in air is
automobile exhaust, so measure should be taken to
stop Pb secretion from this source.
2. Another major problem is the industry.
Solutions to these problems include education
programs directed at the hazards of industry, strict
housing codes to prevent occupancy of hazardous
dwellings and better enforcement of existing safety
standards directed at industry.
Solution/Control of Pb Poisoning
22
1. Moderate lead poisoning may cause GIT
symptom such as constipation, diarrhea, loss of
appetite.
2. At high doses, abdominal pain may occur.
3. Nervous system: The developing CNS of foetus
is the most sensitive target organ for Pb toxic effect. It
may produce in adults.
a. Irritability
b. Fatigue
c. Anorexia
d. Sleep disturbance
e. Headache etc.
Symptoms of Pb-poisoning/Pharmacological action of Pb
23
1. Inorganic lead poisoning: Inorganic lead poisoning
can be cured by treatment with chelating agents
which strongly bind with Ph2+.
a. IV infusion of calcium disodium ethyl diamine
tetra acetic acid (CaNa2EDTA) in combination with
dimercaprol.
b. Long term therapy of oral d-penicillamine is used
for expulsion of Pb from bones.
2. Organic lead poisoning: Initial treatment
consist of decontaminating the skin and preventing
further exposure. If high Pb concentration is present
then epidermic chelation maybe used.
Treatment of Pb toxicity in body
24
1. Pb has a low melting point.
2. It is a soft malleable metal that is easily formed
into a variety of shapes.
3. The chemical activity of Pb causes a protective
coating to form upon exposure to moist air.
4. Pb has the ability to form alloys with many other
metals.
5. The density of Pb is greater than any other
common metal except gold and mercury.
Properties of Pb
25
Source:
1. Some mercury is present in the environment
because it is a naturally occurring element.
2. Electrical and electronic industries in the
manufacture of Hg-vapour, Hg-lamp, fluorescent
tables etc.
3. In the manufacture of vinyl chloride in the
plastic industry
4. Combustion of fossil fuel.
5. Agricultural sources: Organomercurials used as
fungicides for seed dressing.
6. Mercury compounds are dispersed througout
rocks, soil air water and diving organisms by a
complex system of physical, chemical and biological
processes.
Mercury(Hg)
26
Manufacture: Nearly all mercury is produced from the
sulfide (HgS) by means of roasting the are in air
HgS + O2  Hg + SO2
Hg is released as a vapour which is condensed, The
other gases are vented into the atmosphere or
collected.
Properties: The chemical and physical properties of
mercury make it an attractive metal for use in
scientific and industrial / applications. These
properties are-
1. It is liquid at room temperature.
2. It’s freezing point is lowest (-39 C)
3. It has the highest volatility of any metal
4. The electrical resistivity is very low which
makes the Hg as a best metallic electrical conductors.
Mercury(Hg)
27
5. Many metals dissolve in mercury to form amalgams.
6. The metal and its compounds are toxic to all living
organisms.
Pathways of entering Hg into internal environment:
i. By inhalation of mercurial fungicidal and it is
cause chronic poisoning
ii. By skin penetration of methyl mercuric
ointment. It also causes chronic poisoning.
iii. By ingestion of inorganic mercury preparation.
It causes acute poisoning.
Mercury(Hg)
28
Uses:
1. The largest uses are seen to the chlor-alkali
industry which produces, chlorine and caustic soda by
the electrolysis of salt solution.
2. The second greatest use of mercury occurs in
the production of electrical apparatus.
3. Other uses include in the electrical switches
used in the home and mercury batteries.
4. The use of mercury and it’s compounds as
fungicides constituent the 3rd largest category of
mercury consumption.
5. The paper and pulp industry has also many use
of PMA (Phenyl Mercuric Acetate) to prevent the
growth of slime on wet paper pulp during processing
and storage.
Mercury(Hg)
29
6. Agricultural industries use organo-mercury
compound as seed dressing to inhibit the growth of
fungi in agricultural seeds.
7. Elemental or metallic mercury is also used in
thermometer and temperature recording devices
because of long liquid range, uniform and large co-
efficient of thermal expansion and electrical
conductivity.
Organo-mercuric compounds used as seed:
i. Methyl mercury nitrile (CH3-Hg – C=N)
ii. Methyl mercury dicyan diamine (CH3-Hg-NH-
C=NH=NHCN)
iii. Methyl mercury acetate (CH3-Hg-COO-CH3)
iv. Ethyl mercury chloride (C2H5-Hg-Cl)
Mercury(Hg)
30
The primary facts determined are:
1. All mercury compounds are toxic to the body
when present in sufficient quantity.
2. Different mercury compounds exhibit
somewhat different characters of toxicity,
distribution, accumulation and retention in the
body.
3. Certain biological transformation may take
place in the environment or the body which
change mercury compounds of one types into
other types.
Toxic/Detrimental effect of Hg in the body:
Continued
31
4. Mercury binds tightly with sulphur containing groups
in molecules which are present in both enzyme and cell
walls such binding inactivates enzymes and upsets
chemical reactions which they catalyze in the body. The
membrane properties of cell walls are disrupted by the
binding of mercury and normal cellular activities are
inhibited.
5. Mercury vapour is quite/toxic when inhaled. It has
great capacity for diffusion through the lungs into the
blood and then into the brain in which they stored and
lead to serious damage.
32
1. Inorganic mercury tends to accumulate in liver
and kidney tissue. This causes damage but also
provides a means for rapid elimination through the
urinary system.
2. Upon introduction into the body arylmercurials
appear to break down readily into inorganic
mercury compounds and behave as indicated
above. The compound PMA behaves this way.
3. Alkylmercurials represent the greatest health
hazard for a no of reasons:
a) As they diffuse easily through biological
membrane so they easily penetrate into and
accumulate in brain tissue.
Toxic effect of Hg-compound in the body
Continued
33
b) They exhibit long retention times in the body. As a
result the Hg concentration rises even though dosage may
be low.
Symptoms:
Acute-Hg-poisoning
1. Severe GIT irritation
2. Cardiorascular collapse
3. Aneurysm
4. Renal impairment
5. Weakness
6. Headache
7. Insomnia
34
Chronic Hg poisoning
1. Neurologic manifestation such as tremor,
psychosis
2. Mercurial lentis
3. Gingivitis
4. Progressive renal damage
5. Muscle atrophy
Treatment of Hg-poisoning
1. Try to vomiting if enters into body
2. As soon-as Hg intoxication is suspected, IM
injection of dimercaprol or penicillamine is given to
chelate the Hg and accelerate its excretion.
3. Chronic mercury poisoning can be treated by
removing patient from exposure area.
Toxic/Detrimental effect of Hg in the body:
35
1. The chlor alkali industry is the largest industrial
user of mercury. Theoretically, no mercury is
consumed during the process of producing Cl2 or
caustic soda. Some is lost to the products, some leaves
with effluent water and some is lost through air
ventilation system.
2. The paper and pulp industry use PMA to prevent
the growth of slime on wet paper pulp during
processing and storage. The incineration of these
paper produce PMA which is a possible source of
airborne mercury pollution because trace amounts
of mercury remain in such paper.
3. Commercial laundries particularly those with a
diaper service, use PMA to suppress mold.
Source of Hg pollution
36
4. Mercury compounds are used in seed dressings in
agriculture. The amount of mercury in the seed
dressing formulation is small but the effect is large
because the seed dressing is applied to a large
volume of seed that is subsequently sowed over
millions of acres, which results in an extremely
wide spread dissemination of the mercury
compounds.
5. Some mercury is released in the combination of
coal and petroleum products.
6. Sludge from sewage plants also contain enough
mercury, in some cases which make it unsuitable for
use as a soil fertility.
Source of Hg pollution
37
 Arsenic condition is a medical condition caused by
elevated levels of arsenic in the body. The dominant
basis of arsenic poisoning is from ground water
that naturally contains high concentration of
arsenic.
 The recommended limit of arsenic in drinking
water is 0.01 mg/L.
 The recommended forms of arsenic, such as arsenic
trioxide found in drinking water are much more
poisonous than the organic forms.
 Body organs that are usually affected by arsenic
poisoning include skin, lungs, kidneys and liver.
Arsenic poisoning
38
 Headaches
 Confusion
 Drowsiness
 Severe diarrhoea
 Pallor
 Rashes
 Swelling
 Diarrhoea
 Vomiting
 Cramping muscles
 Convulsions
 Stomach pain
 Hair loss
 Blood in the urine (Hematuria)
 Breath that smells like garlic.
Signs and Symptoms of Arsenic pollution
39
 Ground water
 Arsenic containing mineral ores
 Industrial processes
 Semiconductor manufacturing(Gallium arsenide)
 -Fossil fuels
 -Wood treated with arsenic preservatives
 Metallurgy
 -Smelting( Cu, Zn, Pb) and refining of metals and
ores.
 -Gloss manufacturing
 -Commercial products such as Wood preservatives,
Pesticides, Herbicides, Fungicides
 Food( Seafood and fish)
 Others, Antiparasitic drugs, Folk remedies
Source of Arsenic pollution
40
The following measures can help to protect people
from arsenic that gets into groundwater:
 Households having arsenic removal systems this is
a short terms solution that can be adopted until the
arsenic contamination can be dealt with at the
source.
 Testing the water for traces of arsenic.
 Taking care when harvesting rainwater-in areas
where there is high rainfall, arsenic poisoning can
be prevented by ensuring the process of collection
is acceptable.
 The water should not put at risk of infection or
cause to become a breeding ground for mosquitoes.
Prevention of As-poisoning
41
 Well depth-the deeper a well is dug, the less arsenic
in water is likely to have.
 A significant factor of prevention is making people
a ware of the risks. This can be done by educating
populations and workforces about the harmful
effects of arsenic poisoning and how it can be
avoided.
 Another important preventative measure is to have
enough health care staff to check people at risk for
the early signs of arsenic poisoning.
Prevention of As-poisoning
42
 Chelation: Chemical and synthetic methods are
used to treat arsenic poisoning. Dimercaprol and
dimercaptosuccinic acid are chelating agents that
sequester the arsenic away from blood proteins and
are used in treating acute arsenic poisoning.
 Mineral supplements: Supplemental potassium
decreases the risk of life-threatening heart rhythm
problem from arsenic trioxide.
 3. Nutritional intervention: Sulfur containing
substances in garlic scavenge arsenic from tissues
and blood. Concludes that people in areas at risk of
arsenic contamination in the water supply should
eat garlic per day as a preventative.
Treatment of As-poisoning
43
 Removing contaminated clothes and washing
and rinsing skin thoroughly.
 Blood transfusions.
 Bowel irrigation- Passing large quantities of
polyethylene solution through the GI tract to
flush out arsenic.
 Supportive treatment for complications like
heart failure and seizures.
Treatment of As-poisoning
44
Diagnosis of arsenic poisoning over a year can be
measured by studying samples of blood, hair, urine
and fingernail. Urine tests within a day or two after
exposure can help to analyze poisoning at the initial
stage.
 In areas and occupations where there is a risk of
arsenic poisoning, it is important to monitor the
levels of arsenic in the people at risk, by taking
blood, hair, urine and fingernail samples. So we can
say that, Arsenic poisoning can be detected by
diagnostically.
Diagnostic test for As-poisoning
45
 We can detect arsenic poisoning diagnostically by
the following tests:
 Tests in urine and blood: Urine tests would have to
be carried out within 1-2 days of the initial
exposure for making it an accurate indicator of
when the arsenic poisoning occurred. The urine test
is the most reliable test for arsenic exposure within
the last few days. Urine testing needs to be done
within 24-48 hrs for an accurate analysis of an
acute exposure. These tests can also be used to help
diagnose cases where symptoms of arsenic
poisoning are apparent. Tests are available to
diagnosis poisoning by measuring arsenic in blood.
Diagnostic test for As-poisoning
46
 Test in hair and fingernails: To determine the level
of arsenic exposure over a period of up to 12
months, tests on hair and fingernails can be
performed. Although these tests can give an
accurate indication of arsenic exposure levels, they
do not indicate what effects they will have on the
patient’s health. Hair is a potential bioindicator for
arsenic exposure due to it’s ability to store trace
elements from blood. Incorporated elements
maintain their position during growth of hair. Thus
for a temporal estimation of exposure, an assay of
hair composition needs to be carried out with a
single hair which is not possible with older
techniques requiring homogenization and
dissolution of several strands of hair.
Diagnostic test for As-poisoning
47
This type of biomonitoring has been achieved with
newer micro analytical techniques like synchroton-
radiation based X-ray fluorescence spectroscopy and
Micro-particle induced X-ray emission.
Diagnostic test for As-poisoning
48
 Half life of inorganic arsenic in the blood is 10 hrs
and of organic arsenic is around 30 hrs.

 2-4 weeks after the exposure ceases, most of the
remaining arsenic in the body is found in keratin-
rich tissues nails, hair, skin.
 Inorganic arsenic is converted to organic arsenic in
the liver. This may represent a process off
detoxification.
 30-50% of inorganic arsenic is excreted in about 3
days. Both forms are excreted depend on the
acuteness of the exposure and dose.
Toxicokinetics of As-poisoning
49
Trivalent forms:
 bind to sulfahydryl groups leading to inhibition of
enzymatic systems.
 inhibit the kreb’s cycle and oxidative
phosporylation. These lead to inhibition of ATP
production.
 Pentavalent forms:
 can replace the stable phosphate ester bond in ATP
and produce an arsenic ester stable bond.
 Endothelial damage loss of capillary integrity,
capillary leakage.
Patho-physiology of As-poisoning
THANKS TO ALL
50
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52

Environmental Chemistry (1.8.2023) last part.pdf

  • 1.
    1 Monika Rani Saha AssistantProfessor Department of Pharmacy, University of Rajshahi ENVIRONMENTAL CHEMISTRY
  • 2.
    2 Carbon monoxide Carbon monoxide:It is an odourless and colourless gas It is originated in the incomplete combustion of carbonaceous materials. It is highly poisonous gas. Sources: 1. The chief source of CO in atmosphere is combustion due to the automobile exhausts. 2. When coal, wood and oil are burnt, black smoke is produced which contain CO. 3.Cigarette smoke also contain CO.
  • 3.
    3 Continued 4. Some industrialoperation such as electric and blast furnaces, some petroleum refining operations, gas manufacturing plants and mines are contributors of CO to the atmosphere. Effects: 1. Co has a strong affinity for combining with the haemoglobin of the blood to form carboxyhaemoglobin. This reduces the ability of the haemoglobin to carry oxygen to the body tissue. 2. CO also affects the CNS. It is also responsible for heart attacks.
  • 4.
    4 Oxides Of NITROGEN Oxidesof nitrogen are the most abandoned atmospheric contaminant. Sources: 1. Smoke released by automobile engines contains oxides of nitrogen. 2. Highest concentration of NO2 in gaseous emission occurs form industries where nitric acid is produced or used in chemical reaction. 3. In many chemical industries which manufacture explosives and nitrogenous fertilizers also produce oxides of nitrogen.
  • 5.
    5 4. Also presentin tobacco smoke. 5. Large amount of nitrogen oxides are also emitted from power plants. 6. When coal, oil and natural gas undergo combustion at high temperature produce N2 and O2 which upon combination in atmosphere produce NO and NO2 N2 + O2 110℃ 2NO O2 2NO2 Effects: 1. NO2 is very corrosive and affect skin. 2. NO2 helps in formation of smog which causes irritation in eye due to the presence of O3. 3. NO2 provides HNO3 by reacting with rainy water and moisture. 4NO2 + 2H2O + O2  4HNO3 Continued
  • 6.
    6 The HNO3 acidthen comes down as acid rain or acid snow. It makes the lakes so acidic that they can no longer support fish life. The production of agricultural crops is also reduced. 4. It is estimated that eye and nasal irritation will be observed after exposure to about 15 ppm of NO2 and pulmonary discomfort after brief exposure to 25 ppm of NO2. Continued
  • 7.
    7 Continued Hydrocarbons # Chemical compoundswhich contain, C and H is called hydrocarbon. It is denoted by CxH2x+2 # Most motor vehicles and engines are powered by hydrocarbon based fuels such as gasoline and diesel. # Hydrocarbon pollution results when unburned and partially burned fuel emitted from the engine as exhaust and also when fuel evaporates directly into the atmosphere.
  • 8.
    8 Sources: i. Road mobilesources : bus, truck, car etc. ii. Non-road mobile sources : train, marine vehicles, aircraft etc. iii. Others not mobile sources : -agricultural sources, -petroleum -forest fire, -coal Effects: Health impact of hydrocarbons:  Acute respiratory symptoms  Headaches  Vomiting  Brain damage Continued
  • 9.
    9  Reduced cardiovascularfunction  Irritation of eye, nose and throat  Dizziness  Coma  Premature death  Arrhythmia  High concentrations have carcinogenic effects on lungs. (B) Environmental impact of hydrocarbons (i) Major components of smog. (ii) Inhibit plant growth and damage leaf tissues and death of following plants. Continued
  • 10.
    10 Pesticides: A pesticideis a substance or mixture of substance-used to kill pest. A pesticide is any substance intended for preventing, destroying, repelling or migrating any pest. A pesticide may be a chemical substance, biological agent (bacteria, virus), antimicrobial disinfectant or device used against pest. Pest includes- insects plant pathogens, birds, and microbes etc. Source of Pesticides i. Elemental sulphur ii. Toxic chemical (arsenic, lead, mercury) iii. Nicotine sulphate iv. Organochlorine infectant (DDT) v. Triazine and others nitrogen base compound Pesticides
  • 11.
    11  1. Algaecides:The substances which are used for the control of Algae.  2. Avicides: The substances which are used for the control of Birds.  3. Virucides: The substances which are used for the control of viruses.  4. Bactericides: The substances which are used for the control of bacteria.  5. Fungicides: The substances which are used for the control of Fungi.  6. Herbicides: The substances which are used for the control of weeds.  7. Insecticides: The substances which are used for the control of insects. Classification of pesticides
  • 12.
    12 Effects: A) Health effect i)Non-Hodgkin lymphoma is Produced ii) Leukemia iii) Prostate cancer iv) Multiple myeloma and soft tissue sarcoma B) Acute health problem i) Abdominal pain ii) Skin and eye problem iii) Dizziness iv) Nausea v) Vomitting. Pesticides
  • 13.
    13 Cigarattes smoke: Theair pollution by cigarattes is 10 times greater than diesel car exhaust cigarattes contain 4000 chemicals in which 48% is carcinogenic.  Sources: i. Smoke ii. Tiny particles (about 4000 chemicals packed into the cigarattes iii. Additional dangerous product: CO  Effects:  1. Cigarettes smoke contain carcinogenic ingredient such as arsenic tar and CO which damages the lungs function. Cigarettes
  • 14.
    14  2. Nicotineis the additive component contain in cigaratte smoke is also a potent stimulant. It raises blood pressure and increases the heart rate.  3. In regular smoke, nicotine can lead to cardiovascular complications such as enlarge heart arrhythmia and coronary artery diseases.  4. Cigarettes smoke is interfering with the production of insulin which is responsible for allowing blood sugar to enter the body cell.  5. Cigaratte smoke can causes lung cancer Cigarettes
  • 15.
    15 Passive /Involuntary /Second hand smoking: Breathing other people smoke is called passive / Involuntary / Second hand smoking. Effects: i. Eye irritation ii. Headaches iii. Cough iv. Dizziness v. Nausea Those people who regularly inhale other smoke have a 20- 30% greater risk of contracting lung cancer and heart diseases. In children Tobacco smoke is especially dangerous for children. Those who are exposed to basic smoke during early infancy and childhood has a greater risk of bronchitis, preumonia and other chest illness. Cigarettes
  • 16.
    16  Heavy MetalToxicology is the science of study of toxic metals and their mode of action.  These are discharged by industries to air water and soil. They entered into the human food chain from the environment. Once they enter our biological system, they disturb the biochemical processes leading in some cases to fatal results. Factors affecting toxicity:  Route a administration e.g. oral, nasal etc.  ii. Age  iii. Sex  iv. Single or multiple dose  v. Species of the component. Heavy Metal Toxicology
  • 17.
    17  Lead (Pb)is heavy, soft, bluish metal and occurs in nature in the form of ores. Once Pb is mined, processed and introduced into the environment, it is a potential problem forever.  ‘Lead is a highly toxic substance that is harmful when it enters the body. This situation is called lead poisoning. Lead poisoning is preventable and is not contagious. Sources:  1. Burning of fuel in vehicle  2. Industries where lead is extracted.  3. Lead pipes.  4. Tinned food.  5. Decorated candles, coloured photography, hair drier, paints etc. Lead poisoning
  • 18.
    18 The chemical formof Pb is an important factor affecting its biological behavior in the body. 1. Lead is a general protoplasmic poison which accumulates in body and they are slow acting and stable. 2. Organic lead compounds such as tetraethyl lead are readily absorbed by the body through the skin or mucous membranes. This is a serious problem for occupationally exposed workers whose are involved in the manufacture of such compounds. Toxic effect of lead in the body
  • 19.
    19 3. Inorganic leadis absorbed primarily through the gastro-intestinal and respiratory tracts and it is the main source of lead in the body. 4. It obstructs the utilization of O2 and glucose and hinders the production of energy. 5. The toxic action of lead in the body is the enzyme inhibition by the Pb2+ ion. The inhibited enzyme is necessary for the formation of hemoglobin. The inhibition is a result of a strong interaction between Pb2+ and the sulfur groups of some amino acids of the enzyme. Continued
  • 20.
    20 6. The leadretained in the body from both air and dietary source accumulates predominantly in the skeleton . It’s accumulation cause loss of weight, loss of teeth, constipation etc. 7. An unpleasant aspect of bone accumulated lead is that it may be remobilized and sent to other parts of the body long after the initial absorption. This remobilized can occur during feverish illness as a result of cortisone treatment and as a result of old age. Because the determination of lead in bones in difficult, the concentration of lead in blood or urine is commonly used as indication of total lead in the body. Continued
  • 21.
    21 1. Since themajor source of Pb pollution in air is automobile exhaust, so measure should be taken to stop Pb secretion from this source. 2. Another major problem is the industry. Solutions to these problems include education programs directed at the hazards of industry, strict housing codes to prevent occupancy of hazardous dwellings and better enforcement of existing safety standards directed at industry. Solution/Control of Pb Poisoning
  • 22.
    22 1. Moderate leadpoisoning may cause GIT symptom such as constipation, diarrhea, loss of appetite. 2. At high doses, abdominal pain may occur. 3. Nervous system: The developing CNS of foetus is the most sensitive target organ for Pb toxic effect. It may produce in adults. a. Irritability b. Fatigue c. Anorexia d. Sleep disturbance e. Headache etc. Symptoms of Pb-poisoning/Pharmacological action of Pb
  • 23.
    23 1. Inorganic leadpoisoning: Inorganic lead poisoning can be cured by treatment with chelating agents which strongly bind with Ph2+. a. IV infusion of calcium disodium ethyl diamine tetra acetic acid (CaNa2EDTA) in combination with dimercaprol. b. Long term therapy of oral d-penicillamine is used for expulsion of Pb from bones. 2. Organic lead poisoning: Initial treatment consist of decontaminating the skin and preventing further exposure. If high Pb concentration is present then epidermic chelation maybe used. Treatment of Pb toxicity in body
  • 24.
    24 1. Pb hasa low melting point. 2. It is a soft malleable metal that is easily formed into a variety of shapes. 3. The chemical activity of Pb causes a protective coating to form upon exposure to moist air. 4. Pb has the ability to form alloys with many other metals. 5. The density of Pb is greater than any other common metal except gold and mercury. Properties of Pb
  • 25.
    25 Source: 1. Some mercuryis present in the environment because it is a naturally occurring element. 2. Electrical and electronic industries in the manufacture of Hg-vapour, Hg-lamp, fluorescent tables etc. 3. In the manufacture of vinyl chloride in the plastic industry 4. Combustion of fossil fuel. 5. Agricultural sources: Organomercurials used as fungicides for seed dressing. 6. Mercury compounds are dispersed througout rocks, soil air water and diving organisms by a complex system of physical, chemical and biological processes. Mercury(Hg)
  • 26.
    26 Manufacture: Nearly allmercury is produced from the sulfide (HgS) by means of roasting the are in air HgS + O2  Hg + SO2 Hg is released as a vapour which is condensed, The other gases are vented into the atmosphere or collected. Properties: The chemical and physical properties of mercury make it an attractive metal for use in scientific and industrial / applications. These properties are- 1. It is liquid at room temperature. 2. It’s freezing point is lowest (-39 C) 3. It has the highest volatility of any metal 4. The electrical resistivity is very low which makes the Hg as a best metallic electrical conductors. Mercury(Hg)
  • 27.
    27 5. Many metalsdissolve in mercury to form amalgams. 6. The metal and its compounds are toxic to all living organisms. Pathways of entering Hg into internal environment: i. By inhalation of mercurial fungicidal and it is cause chronic poisoning ii. By skin penetration of methyl mercuric ointment. It also causes chronic poisoning. iii. By ingestion of inorganic mercury preparation. It causes acute poisoning. Mercury(Hg)
  • 28.
    28 Uses: 1. The largestuses are seen to the chlor-alkali industry which produces, chlorine and caustic soda by the electrolysis of salt solution. 2. The second greatest use of mercury occurs in the production of electrical apparatus. 3. Other uses include in the electrical switches used in the home and mercury batteries. 4. The use of mercury and it’s compounds as fungicides constituent the 3rd largest category of mercury consumption. 5. The paper and pulp industry has also many use of PMA (Phenyl Mercuric Acetate) to prevent the growth of slime on wet paper pulp during processing and storage. Mercury(Hg)
  • 29.
    29 6. Agricultural industriesuse organo-mercury compound as seed dressing to inhibit the growth of fungi in agricultural seeds. 7. Elemental or metallic mercury is also used in thermometer and temperature recording devices because of long liquid range, uniform and large co- efficient of thermal expansion and electrical conductivity. Organo-mercuric compounds used as seed: i. Methyl mercury nitrile (CH3-Hg – C=N) ii. Methyl mercury dicyan diamine (CH3-Hg-NH- C=NH=NHCN) iii. Methyl mercury acetate (CH3-Hg-COO-CH3) iv. Ethyl mercury chloride (C2H5-Hg-Cl) Mercury(Hg)
  • 30.
    30 The primary factsdetermined are: 1. All mercury compounds are toxic to the body when present in sufficient quantity. 2. Different mercury compounds exhibit somewhat different characters of toxicity, distribution, accumulation and retention in the body. 3. Certain biological transformation may take place in the environment or the body which change mercury compounds of one types into other types. Toxic/Detrimental effect of Hg in the body:
  • 31.
    Continued 31 4. Mercury bindstightly with sulphur containing groups in molecules which are present in both enzyme and cell walls such binding inactivates enzymes and upsets chemical reactions which they catalyze in the body. The membrane properties of cell walls are disrupted by the binding of mercury and normal cellular activities are inhibited. 5. Mercury vapour is quite/toxic when inhaled. It has great capacity for diffusion through the lungs into the blood and then into the brain in which they stored and lead to serious damage.
  • 32.
    32 1. Inorganic mercurytends to accumulate in liver and kidney tissue. This causes damage but also provides a means for rapid elimination through the urinary system. 2. Upon introduction into the body arylmercurials appear to break down readily into inorganic mercury compounds and behave as indicated above. The compound PMA behaves this way. 3. Alkylmercurials represent the greatest health hazard for a no of reasons: a) As they diffuse easily through biological membrane so they easily penetrate into and accumulate in brain tissue. Toxic effect of Hg-compound in the body
  • 33.
    Continued 33 b) They exhibitlong retention times in the body. As a result the Hg concentration rises even though dosage may be low. Symptoms: Acute-Hg-poisoning 1. Severe GIT irritation 2. Cardiorascular collapse 3. Aneurysm 4. Renal impairment 5. Weakness 6. Headache 7. Insomnia
  • 34.
    34 Chronic Hg poisoning 1.Neurologic manifestation such as tremor, psychosis 2. Mercurial lentis 3. Gingivitis 4. Progressive renal damage 5. Muscle atrophy Treatment of Hg-poisoning 1. Try to vomiting if enters into body 2. As soon-as Hg intoxication is suspected, IM injection of dimercaprol or penicillamine is given to chelate the Hg and accelerate its excretion. 3. Chronic mercury poisoning can be treated by removing patient from exposure area. Toxic/Detrimental effect of Hg in the body:
  • 35.
    35 1. The chloralkali industry is the largest industrial user of mercury. Theoretically, no mercury is consumed during the process of producing Cl2 or caustic soda. Some is lost to the products, some leaves with effluent water and some is lost through air ventilation system. 2. The paper and pulp industry use PMA to prevent the growth of slime on wet paper pulp during processing and storage. The incineration of these paper produce PMA which is a possible source of airborne mercury pollution because trace amounts of mercury remain in such paper. 3. Commercial laundries particularly those with a diaper service, use PMA to suppress mold. Source of Hg pollution
  • 36.
    36 4. Mercury compoundsare used in seed dressings in agriculture. The amount of mercury in the seed dressing formulation is small but the effect is large because the seed dressing is applied to a large volume of seed that is subsequently sowed over millions of acres, which results in an extremely wide spread dissemination of the mercury compounds. 5. Some mercury is released in the combination of coal and petroleum products. 6. Sludge from sewage plants also contain enough mercury, in some cases which make it unsuitable for use as a soil fertility. Source of Hg pollution
  • 37.
    37  Arsenic conditionis a medical condition caused by elevated levels of arsenic in the body. The dominant basis of arsenic poisoning is from ground water that naturally contains high concentration of arsenic.  The recommended limit of arsenic in drinking water is 0.01 mg/L.  The recommended forms of arsenic, such as arsenic trioxide found in drinking water are much more poisonous than the organic forms.  Body organs that are usually affected by arsenic poisoning include skin, lungs, kidneys and liver. Arsenic poisoning
  • 38.
    38  Headaches  Confusion Drowsiness  Severe diarrhoea  Pallor  Rashes  Swelling  Diarrhoea  Vomiting  Cramping muscles  Convulsions  Stomach pain  Hair loss  Blood in the urine (Hematuria)  Breath that smells like garlic. Signs and Symptoms of Arsenic pollution
  • 39.
    39  Ground water Arsenic containing mineral ores  Industrial processes  Semiconductor manufacturing(Gallium arsenide)  -Fossil fuels  -Wood treated with arsenic preservatives  Metallurgy  -Smelting( Cu, Zn, Pb) and refining of metals and ores.  -Gloss manufacturing  -Commercial products such as Wood preservatives, Pesticides, Herbicides, Fungicides  Food( Seafood and fish)  Others, Antiparasitic drugs, Folk remedies Source of Arsenic pollution
  • 40.
    40 The following measurescan help to protect people from arsenic that gets into groundwater:  Households having arsenic removal systems this is a short terms solution that can be adopted until the arsenic contamination can be dealt with at the source.  Testing the water for traces of arsenic.  Taking care when harvesting rainwater-in areas where there is high rainfall, arsenic poisoning can be prevented by ensuring the process of collection is acceptable.  The water should not put at risk of infection or cause to become a breeding ground for mosquitoes. Prevention of As-poisoning
  • 41.
    41  Well depth-thedeeper a well is dug, the less arsenic in water is likely to have.  A significant factor of prevention is making people a ware of the risks. This can be done by educating populations and workforces about the harmful effects of arsenic poisoning and how it can be avoided.  Another important preventative measure is to have enough health care staff to check people at risk for the early signs of arsenic poisoning. Prevention of As-poisoning
  • 42.
    42  Chelation: Chemicaland synthetic methods are used to treat arsenic poisoning. Dimercaprol and dimercaptosuccinic acid are chelating agents that sequester the arsenic away from blood proteins and are used in treating acute arsenic poisoning.  Mineral supplements: Supplemental potassium decreases the risk of life-threatening heart rhythm problem from arsenic trioxide.  3. Nutritional intervention: Sulfur containing substances in garlic scavenge arsenic from tissues and blood. Concludes that people in areas at risk of arsenic contamination in the water supply should eat garlic per day as a preventative. Treatment of As-poisoning
  • 43.
    43  Removing contaminatedclothes and washing and rinsing skin thoroughly.  Blood transfusions.  Bowel irrigation- Passing large quantities of polyethylene solution through the GI tract to flush out arsenic.  Supportive treatment for complications like heart failure and seizures. Treatment of As-poisoning
  • 44.
    44 Diagnosis of arsenicpoisoning over a year can be measured by studying samples of blood, hair, urine and fingernail. Urine tests within a day or two after exposure can help to analyze poisoning at the initial stage.  In areas and occupations where there is a risk of arsenic poisoning, it is important to monitor the levels of arsenic in the people at risk, by taking blood, hair, urine and fingernail samples. So we can say that, Arsenic poisoning can be detected by diagnostically. Diagnostic test for As-poisoning
  • 45.
    45  We candetect arsenic poisoning diagnostically by the following tests:  Tests in urine and blood: Urine tests would have to be carried out within 1-2 days of the initial exposure for making it an accurate indicator of when the arsenic poisoning occurred. The urine test is the most reliable test for arsenic exposure within the last few days. Urine testing needs to be done within 24-48 hrs for an accurate analysis of an acute exposure. These tests can also be used to help diagnose cases where symptoms of arsenic poisoning are apparent. Tests are available to diagnosis poisoning by measuring arsenic in blood. Diagnostic test for As-poisoning
  • 46.
    46  Test inhair and fingernails: To determine the level of arsenic exposure over a period of up to 12 months, tests on hair and fingernails can be performed. Although these tests can give an accurate indication of arsenic exposure levels, they do not indicate what effects they will have on the patient’s health. Hair is a potential bioindicator for arsenic exposure due to it’s ability to store trace elements from blood. Incorporated elements maintain their position during growth of hair. Thus for a temporal estimation of exposure, an assay of hair composition needs to be carried out with a single hair which is not possible with older techniques requiring homogenization and dissolution of several strands of hair. Diagnostic test for As-poisoning
  • 47.
    47 This type ofbiomonitoring has been achieved with newer micro analytical techniques like synchroton- radiation based X-ray fluorescence spectroscopy and Micro-particle induced X-ray emission. Diagnostic test for As-poisoning
  • 48.
    48  Half lifeof inorganic arsenic in the blood is 10 hrs and of organic arsenic is around 30 hrs.   2-4 weeks after the exposure ceases, most of the remaining arsenic in the body is found in keratin- rich tissues nails, hair, skin.  Inorganic arsenic is converted to organic arsenic in the liver. This may represent a process off detoxification.  30-50% of inorganic arsenic is excreted in about 3 days. Both forms are excreted depend on the acuteness of the exposure and dose. Toxicokinetics of As-poisoning
  • 49.
    49 Trivalent forms:  bindto sulfahydryl groups leading to inhibition of enzymatic systems.  inhibit the kreb’s cycle and oxidative phosporylation. These lead to inhibition of ATP production.  Pentavalent forms:  can replace the stable phosphate ester bond in ATP and produce an arsenic ester stable bond.  Endothelial damage loss of capillary integrity, capillary leakage. Patho-physiology of As-poisoning
  • 50.
  • 51.
  • 52.