Specific Air Pollutants

5 major substances that account for 98% of air pollution

1. Carbon monoxide: CO; 52%
2. Sulfur Oxides: 14%
3. Hydrocarbons 14%
4. Nitrogen Oxides 14%
5. Particulate matter 4%
Sources:
1. Transportation
2. Industry
3. Generation of electric power
4. Space heating
5. REfuse disposal
CLinical impact:
- Sulfur dioxide and smoke from incomplete combustion- acute adverse effects among the elderly
and individuals with preexisting cardiac and respiratory disease
-Ambient air pollution: bronchitis, obstructive ventilatory disease, emphysema, bronchial asthma
and lung cancer

CARBON MONOXIDE:
-Colorless, tasteless, odorless and non irrietating gas
-by product of incomplete combustion
-average concentration: 0.1ppm; exceeds exceeds 100ppm in heavy traffic
MOA:
-CO combines reversibly with O2 binding sites if Hb
220 times greater affinity with Hb than with O2
-Carboxyhemoglobin:
cannot transport O2
interferes with dissociation of oxygen from remining oxyHb
reduced transfrer of O2 to tissues
-Brain and heart are the organs most affected
-normal non smoking adults have less than 1% CO saturation (1% of total Hb is in the form of
COHb
-Smokers: 5-10% saturation
-a person breathing air with 0.1%CO (1000ppm) would have COHb kevek of about 50%
CLINICAL EFFECTS:
-Principal sign is hypoxia which progress in the following sequence
a. Psychomotor impairment
b. Headache and tightness in temporal area
c. Confusion and loss of visual acuity
d. Tachycardia, tachypnea, syncope and coma
e. Deep coma, convulsions, shock and respiratory failure
levels of COHb and clinical presentation
15% eadache and malaise
25% headache, fatigue, decreased attention span loss of motor coordintion
40% collapse and syncope
 60% death due to irreversible damage to the brarin and myocardium
CLinical effects aggravated by heavy labor, high altitude and high ambient
temperatures
Chronic exposure to low levels of CO may lead to atherosclerotic coronary disease in
cigarette smokers
TREATMENT:
Acute intoxication: Remove individual from the exposure source and maintain
respiration followed by O2 administration
Half time of CO elimination
-Room air (1atm): 320 minutes
-100% O2 80 minutes
-hyperbaric O2 (2-3atm) 20 mins (hyperbaric O2 chamber)
-recovery is often cmplete

-SULLFUR DIOXIDE:
-COlorless irritant gas
-generated by combustion of sulfur containing fossil fuels
MOA:
-SO2 forms sulfurous acid - irritant effects on eyes, mcus membranes and skin
-90% of inhaled SO2 is absorbed in the upper resp tract
-effects:
bronchial constriction
-Parasympathetic reflexes
altered SM tone
5ppm SO2 for 10 mins: increased resisttance to air flow
5-10ppm: severe bronchospasm
Asthmatic individuals are especially sensitive to SO2
`CLINICAL EFFECTS AND TREATMENT:
-irritation of the eyes, nose and throat and reflex bronchoconstriction
-Among asthmatics, SO2 exposure may result in acute asthmatic episode. Severe exposure may
result in delayed onset pulmonary edema
Treatment is not specific for SO2 but is directed at treatment of the irritation of respiratory tract
and asthma
NITROGEN OXIDES:
-Nitrogen Dioxide (NO2): brownish irritant gas sometimes associated with fires
MOA: Relatively insoluble deep lung irritant capable of producing pulmonary edema
-Type 1 cells of alveoli are chiefly affected on acute exposure
-At higher exposures, type I and II are affected
25ppm of NO2: irritation
50ppm moderately irritating to the eyes and nose
1 hour at 50ppm can cause pulmonary edema
100ppm can ause pulmonary edema and death
CLINICAL EFFECTS AND TREATMENT:
1st stage:
-Irritation to eyes and nose, cough, mucoid or frothy sputum production
-dyspnea and chest pain
 -pulmonary edema within 1-2 hours
-may subside in some individuals in 2 weeks
2nd stage:
-increased severity of signs and symptoms with recurring pulmonary edema and fibrotic destruction
of terrminal bronchioles (Bronchiolitis obliterans)
-No specific treatment- treat pulmonary edema, maintain gas exchange with adequate O2
OZONE (O3):
-Bluish irritant gas, normal in the earths atmosphere- absorbs UV light
-Workplace:
High voltage electrical equipment
Ozone producing devices used for air and water purification
MOA:
-Irritant of mucus membranes
Mild exposure: URT irritation
Severe exposure: deep lung irritation with pulmonary edema
*exercise increases the amount of O3 reaching the lungs
0.1ppm for 10-30 mins: irritation and dryness of the throat
>0.1ppm:changesin visual acuity, substernal pain and dyspnea
Variety of effects: Chronic bronchitis
Bronchilitis
Fibrosis
Emphysematous changes
-No specific treatment: treat lung irritation and pulmonary edema
HYDROCARBONS:
1. Halogenated aliphatic hydrocarbons:
-Source: industrial solvents, degreasing agents, cleaning agents
CCL4,
Chloroform,
Percholoroethylene and Tricholoroethylene
used in dry cleaning, carcinogens that when improperly disposed seeps into
ground water
-Carcinogen, renal, testicular, prostate
MOA: CNS depression (Chloroform is most potent)
Liver toxicity
Kidney injury
Cardiotoxicity
Carcinogens
Treated according to the system involved
2. Benzene: important component of gasoline, may be as high as 2% in premium gasoline
-as much as 5% in cold climates likes Alaska
-PEL is 1ppm in air, 5ppm for skin exposure (further reduced to 0.1ppm)
-Acute toxic effect: CNS depression
7500ppm for 30 mins:: fatal
>3000ppm: euphoria, nausea, locomotor problems and coma
250-500ppm: vertigo, drowsiness, headache and nausea
-Chronic exposure: serious toxic effects
Bone marrow injury is most significant
Aplastic anemia, leucopenia, pancytopenia and thrombocytopenia, Leukemia
Lymphoma, myeloma,
3. Tolouene (Methylbenzene):
-CNS depressant, skin and eye irritant, fetotoxic
800ppm: severe fatigue and ataxia
10Kppm: rapid loss of consciousness
4. Xylene (dimethylbenzene):
-substituted for benzene as a degreasing agent]
2. Aromatic Hydrocarbons:
a. Benzene: used for its solvent properties
-important component of gasoline (as high as 2% in premium)
-PEL 1ppm in the air and 5ppm for sin exposure (others recommend 0.1ppm)
-Effect: CNS depression
-Acute exposure
7500ppm for 30 mins can be fatal
>3000ppm causes euphoria, nausea and locomotor problems and coma
250-500ppm vertigo, drowsiness, headache, nausea
-Chronic exposure:
BM injury- most tsignificant
Aplastic anemia, leucopenia, pancytopenia, thrombocytopenia, leukemia
b. Toluene: (Methylbenzene)
-no myelotoxic properties as benzene, not associated with leukemia
Effect: CNS depressant, skin and eye irritant
800ppm- severe fatigue and ataxia
10,000ppm- rapid loss of consciousness
c. Xylene: (dimethylbenzene)
-benzene substitute in solvent degreasing
Effect: CNS depressant and skin irritant
No myelotoxic property and not associated with leukemia
Effect: CNS depressant, skin and eye irritant