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2S - PCT > 5.1 Intro to Toxi: Air Pollutants > Flashcards

5.1 Intro to Toxi: Air Pollutants Flashcards

1
Q

5 Major Air Pollutants in industrialized countries

A
  • carbon monoxide (CO) (which accounts for about 50% of the total amount of air pollutants)
  • sulfur oxides (18%)
  • hydrocarbons (12%)
  • particulate matter (eg, smoke particles,10%)
  • nitrogen oxides (6%).
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2
Q

Air pollution appears to be a contributing factor in (3)

A
  1. bronchitis
  2. obstructive pulmonary disease
  3. lung cancer
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3
Q

Air contaminants are regulated in the United States by the _______.

A

Environmental Protection Agency (EPA)

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4
Q

Air pollutant that is:

Colorless, tasteless, odorless and non-irritating gas. Silent Killer. Individuals found dead within their vehicles with no struggle

A

CARBON MONOXIDE (CO)

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5
Q

Air pollutant that is:

Byproduct of incomplete combustion. gas stoves; generators and other gasoline powered equipment; automobile exhaust and tobacco smoke

A

CARBON MONOXIDE (CO)

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6
Q

Air pollutant that is:

Easily absorbed through the lungs. Exposure may be acute or chronic. Has teratogenic potential

A

CARBON MONOXIDE (CO)

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6
Q

Air pollutant:

T/F: Since vapes have heating devices in them, they can also produce carbon monoxide.

A

T

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7
Q

Air pollutant that is:

competes avidly with oxygen for hemoglobin.

A

CARBON MONOXIDE (CO)

The affinity of CO for hemoglobin is more than 200fold greater than that of oxygen

The threshold limit value of CO for an 8h workday is 25 parts per million (ppm); in heavy motor vehicle traffic, the concentration of CO may exceed 100 ppm.

CO is slightly lighter than air but mixes homogeneously in room air

CO < Air
CO = Room Air

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8
Q

Effect - Air pollutant that is:

causes tissue hypoxia

Headache occurs first,
followed by confusion, decreased visual acuity, tachycardia, syncope, coma, seizures, and death.

A

CARBON MONOXIDE (CO)

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9
Q

Effect - Air pollutant that is:

Collapse and syncope occur when approximately 40% of hemoglobin has been converted to carboxyhemoglobin.

A

CARBON MONOXIDE (CO)

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10
Q

CARBON MONOXIDE (CO):
Prolonged hypoxia can result in irreversible damage to the ______ and the _______.

A

brain and myocardium

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11
Q

CARBON MONOXIDE (CO):
T/F: Exposure of a pregnant woman to elevated CO levels at critical fetal developmental periods may cause
fetal death or serious and irreversible but survivable birth defects.

A

T

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12
Q

Sources at home - Air pollutant that is:

Car left running in attached garage

A

CARBON MONOXIDE (CO)

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13
Q

Sources at home - Air pollutant that is:

Clogged chimney, Corroded or disconnected water heater vent pipe, Gas or wood-burning fireplace, Cracked or loose furnace exchanger

A

CARBON MONOXIDE (CO)

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14
Q

Sources at home - Air pollutant that is:

Improperly installed kitchen range or vent, Operating a grill indoors or in garage, Portable kerosene or gas heaters

A

CARBON MONOXIDE (CO)

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15
Q

Mechanism of Action - Air pollutant that is:

______ combines tightly but reversibly with the oxygen
binding site of hemoglobin (Hb)

A

CARBON MONOXIDE (CO)

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16
Q

Mechanism of Action - Air pollutant that is:

Produces Carboxyhemoglobin. Their blood becomes cherry-red

A

CARBON MONOXIDE (CO)

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16
Q

Air pollutant that is:

Source from burning of coal; power plants

A

SULFUR DIOXIDE (SO2)

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16
Q

Mechanism of Action - Air pollutant that is:

CO affinity 220x oxygen. CO has a higher affinity to bind compared
to oxygen

A

CARBON MONOXIDE (CO)

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17
Q

Mechanism of Action - Air pollutant that is:

Reduced oxygen transfer to the tissues. Organs with the highest oxygen demand are most seriously affected (Brain, Heart and Kidneys)

A

CARBON MONOXIDE (CO)

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18
Q

Mechanism of Action - Carbon Monoxide

T/F: Homoglobin carries oxygen and carbon dioxide. Carbon monoxide then binds very tightly to hemoglobin; thus, oxygen and carbon dioxide can no longer be carried

A

T

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18
Q

Mechanism of Action - Carbon Monoxide
What are the prgans with the highest oxygen demand and are most seriously affected (3)

A

(Brain, Heart and Kidneys)

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19
Q

CLINICAL EFFECTS:

Symptoms of tissue hypoxia

A

CARBON MONOXIDE (CO)

Causes hypoxia because instead of oxygen
being bound to hemoglobin then delivered
to tissues, it is carbon monoxide instead.

It displaces oxygen and carbon monoxide becomes circulated in the blood.

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20
Q

CLINICAL EFFECTS:

Psychomotor impairment

Reflexes are obtunded and gone.

A

CARBON MONOXIDE (CO)

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21
Q

CLINICAL EFFECTS:

When awake:
○ Headache and tightness in the temporal area
○ Confusion and loss of visual acuity

A

CARBON MONOXIDE (CO)

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21
Q

CLINICAL EFFECTS:
Tachycardia, tachypnea, syncope, and coma

The heart will try to compensate due to
hypoxia (lack of oxygen); the heart will
pump faster and harder. Eventually, they
lose consciousness.

A

CARBON MONOXIDE (CO)

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22
Q

CARBON MONOXIDE (CO) is Aggravated by (5)

A
  1. Heavy Labor
  2. High Altitude
  3. High ambient temperature
  4. Smoking Exposure
  5. Cardiorespiratory diseases

HEAVY LOAD: Ex. construction workers who carry heavy loads. They have a higher oxygen requirement, so they are easier to succumb to carbon monoxide poisoning.

HIGH ALTITUDE: Mountains, construction of high rise buildings

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22
Q

TREATMENT FOR CARBON MONOXIDE (CO)

A
  1. First step: Remove victim from source of CO
  2. 100% Oxygen is the specific antidote/antagonist for CO
  3. High concentrations of oxygen for a short amount of time only
  4. Hypothermic therapy
  5. Neuropsychological and motor dysfunction persists for a long time after treatment
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22
Q

CLINICAL EFFECTS:

Deep coma, convulsions, shock and respiratory
failure

Dies from respiratory failure

A

CARBON MONOXIDE (CO)

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23
Q

Air pollutant that is:

Colorless irritant gas

Upper respiratory tract irritant. Irritating (ex. Causes eyes to water) like when muriatic acid evaporates

A

SULFUR DIOXIDE (SO2)

24
Q

Air pollutant that is:

Sulfuric Acid (used to clean in bathrooms)

Irritates nasal mucosa, pharynx, and larynx upon inhalation (causing cough)

A

SULFUR DIOXIDE (SO2)

25
Q

Air pollutant that is:

Principal source is the burning of coal, domestic heating, high-sulfur transportation and coal-fired power plants

A

SULFUR DIOXIDE (SO2)

25
Q

Air pollutant that is:

Generated primarily by the combustion of sulfur-containing fossil fuel

A

SULFUR DIOXIDE (SO2)

26
Q

Air pollutant that is: (Mechanism of Action)

It readily dissolves in our mucosa (sa nasopharynx) to produce the sulfurous acid which causes the irritation in our mucosa

A

SULFUR DIOXIDE (SO2)

27
Q

Air pollutant that is: (Mechanism of Action)

High solubility of SO2 in moist membranes forms sulfurous acid

A

SULFUR DIOXIDE (SO2)

28
Q

Air pollutant that is: (Mechanism of Action)

It readily dissolves in our mucosa (sa nasopharynx) to produce the sulfurous acid which causes the irritation in our mucosaSevere irritant on the eyes, mucous membranes,
respiratory tract and skin

A

SULFUR DIOXIDE (SO2)

29
Q

Air pollutant that is: (Mechanism of Action)

Severe irritant on the eyes, mucous membranes,
respiratory tract and skin

A

SULFUR DIOXIDE (SO2)

30
Q

Air pollutant that is: (Mechanism of Action)

90% of inhaled form is absorbed in the Upper
Respiratory Tract causing Acute Irritant Asthma

When the bronchus constricts, it makes breathing even more difficult because the airway is too small

A

SULFUR DIOXIDE (SO2)

31
Q

Air pollutant that is: (Mechanism of Action)

The phenomenon of adapting to irritating concentrations has been reported in workers

  • Some workers show the phenomenon of adaptation when they have been exposed for too long
  • They almost seem immune to it, Needs gas mask when exposed
A

SULFUR DIOXIDE (SO2)

32
Q

Air pollutant that is: (CLINICAL EFFECTS)

May initiate or exacerbate Bronchial Asthma

A

SULFUR DIOXIDE (SO2)

33
Q

Air pollutant that is: (CLINICAL EFFECTS)

Eye, nose, and throat irritation, reflex bronchoconstriction and increased bronchial secretions

  • Bronchoconstriction = nahihirapan huminga
  • Presence of 5–10 ppm in the air is enough to cause severe bronchospasm
A

SULFUR DIOXIDE (SO2)

34
Q

Air pollutant that is: (CLINICAL EFFECTS)

Delayed-onset pulmonary edema

Thickening of the blood air barrier, making it more difficult to breathe

A

SULFUR DIOXIDE (SO2)

35
Q

Air pollutant that is: (TREATMENT)

  • Treatment is supportive, non-specific
  • Removal from exposure to SO2 and relief of irritation and inflammation constitute major treatment
  • Oxygenation, bronchodilation, mucolytics (reduces mucus secretions)
A

SULFUR DIOXIDE (SO2)

35
Q

Air pollutant that is:

  • Exhaust of vehicles
  • Automobile and truck traffic emissions
  • Brownish irritant gas associated with fires
A

NITROGEN OXIDES (NO2)

36
Q

Air pollutant that is:

  • Farmers exposed to fresh silage

Leftover harvest is burned (husks)

A

NITROGEN OXIDES (NO2)

37
Q

Air pollutant that is:

  • Miners exposed to diesel equipment

  • Required to have engines be cleaned very often so as not to produce too much NO2
  • Causes smog in atmosphere
A

NITROGEN OXIDES (NO2)

38
Q

Air pollutant that is: (MECHANISM OF ACTION)

  • ## Relatively insoluble deep lung irritant

Not much in airways, but more in alveoli

A

NITROGEN OXIDES (NO2)

39
Q

Air pollutant that is: (MECHANISM OF ACTION)

  • Inhalation damages the lung infrastructure that produces the surfactant necessary to allow smooth and low-effort lung alveolar expansion

  • Decreases the surfactant which is what maintains the patency of alveoli
  • Without surfactant, the alveoli will stick to each other
  • Dissolves the surfactant
A

NITROGEN OXIDES (NO2)

40
Q

In NITROGEN OXIDES (NO2):

Nitric Oxide is

  • NO
  • NO2
  • N2O
40
Q

In NITROGEN OXIDES (NO2):

Nitrogen dioxide is

  • NO
  • NO2
  • N2O
41
Q

In NITROGEN OXIDES (NO2):

Nitrous oxide is

  • NO
  • NO2
  • N2O
42
Q

Air pollutant that is: (CLINICAL EFFECTS)

  • Silo-Filler’s Disease, Non-allergic Asthma, ”Twitchyairway disease”
A

NITROGEN OXIDES (NO2)

43
Q

NITROGEN OXIDES (NO2): CLINICAL EFFECTS

If you are chronically working in agriculture areas (Silo worker), the fumes can cause _________ or the destruction of the alveolar cell walls

44
Q

Air pollutant that is: (CLINICAL EFFECTS)

  • Acute: Irritation of eyes and nose, cough, mucoid or frothy sputum production, dyspnea and chest pain; Pulmonary edema, fibrotic destruction of terminal bronchioles
A

NITROGEN OXIDES (NO2)

45
Q

Air pollutant that is: (CLINICAL EFFECTS)

  • Chronic: Emphysematous changes

Entailing damage already in the alveoli

A

NITROGEN OXIDES (NO2)

46
Q

Air pollutant that is: (Treatment)

  • Chronic: Supportive, non-specific
A

NITROGEN OXIDES (NO2)

47
Q

Air pollutant that is:

  • Bluish irritant gas naturally found in the earth’s atmosphere
  • Burning of fossil fuel
  • Emitted from power plants, motor vehicles and other sources of high heat compounds
  • High-voltage electrical equipment and air and water purification systems

It is heavier than air.

produced in air and water purification devices and in electrical fields.

A

OZONE (O3) & OTHER OXIDES

48
Q

Sources of Ozone:

A

● Area sources
● Point sources
● Non-road engines
● Oil and gas
● Biogenic sources
● Off-road engines (Aviation)
● On-road vehicles

49
Q

Mechanism of Action of Ozone:

A

● Irritant of mucous membranes
● Produces upper respiratory tract irritation to deep lung irritation with pulmonary edema
● Formation of reactive free radicals

Free radicals - reactive oxygen species having an unpaired electron.

It would be like a chain reaction. It oxidizes all chemicals in the area where it is located. This is where antioxidants start to become crucial, because they neutralize unpaired electrons -> (Some vitamins, like glutathione, have antioxidants.) Hindi kasi matatapos until ‘di mareceive ung electrons, mag-ch-chain reaction until
mareceive

50
Q

Air pollutant that is: (Mechanism of Action)

  • Irritant of mucous membranes
  • Produces upper respiratory tract irritation to deep lung irritation with pulmonary edema
  • Formation of reactive free radicals
51
Q

Clinical Effects of Action of Ozone:

A
  • Shallow, rapid breathing and decrease in pulmonary compliance
  • Exposure to 0.01–0.1 ppm may cause irritation and dryness of the mucous membranes.
  • Acute: Irritation and dryness to throat, changes to visual acuity, substernal pain and dyspnea, ARDS
  • Chronic: Chronic Bronchitis, Bronchiolitis, Emphysema
52
Q

Air pollutant that is: Clinical Effects

  • Shallow, rapid breathing and decrease in pulmonary compliance
  • Exposure to 0.01–0.1 ppm may cause irritation and dryness of the mucous membranes.
53
Q

Air pollutant that is: Clinical Effects

  • Acute: Irritation and dryness to throat, changes to visual acuity, substernal pain and dyspnea, ARDS

Exacerbate respiratory diseases:
- Chronic: Chronic Bronchitis, Bronchiolitis, Emphysema

End stage of respiratory diseases: emphysema

54
Q

Air pollutant that is: Treatment

Supportive, non-specific
The dose needs to be lowered

55
Q

Air Pollutants

High solubility of SO2 in moist membranes forms

A

sulfurous acid

56
Q

Air Pollutants

Severe irritant on the eyes, mucous membranes, respiratory tract and skin

A

sulfurous acid

57
Q

Air Pollutants

T/F 90% of inhaled form of SO2 is absorbed in the Lower Respiratory tract causing Acute Irritant Asthma

A

F; Upper Respiratory Tract

58
Q

Air Pollutants

Clinical Effects include Eye, nose and throat irritation, reflex bronchoconstriction and increased bronchial secretions

A

Sulfur Dioxide (SO2)

59
Q

Air Pollutants

Treatment is supportive, non-specific

A

Sulfur Dioxide (SO2), Nitrogen Oxides (NO2)

60
Q

Air Pollutants

T/F Surfactant maintains the patency of our alveoli, if not the alveoli will stick to one another

61
Q

Air Pollutants

Brownish irritant gas associated with fires

A

Nitrogen Oxides (NO2)

61
Q

Air Pollutants

  • May initiate or exacerbate Bronchial Asthma
  • Delayed-onset pulmonary edema
A

Sulfur Dioxide (SO2)

62
Q

Air Pollutants (MOA)

T/F Inhalation damages the lung infrastructure that produces the surfactant necessary to allow smooth and low-eort lung alveolar expansion

2S - PCT (12 decks)

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