Air Pollution

EPA Standards

National Ambient Air Quality Standards (NAAQS)

Standards are set for 6  pollutants ("Criteria" pollutants)

1. Particulate matter based on size (PM10 and PM 2.5)
2. Ground-level ozone (O3) (bad ozone-more problems than upper level ozone)
3. Carbon monoxide (CO)
4. Sulfer dioxide (SO2)
5. Nitrogen dioxide (NO2)
6. Lead-from gas components now phased out

Air Pollution 

Particulate Matter

• PM10 = inhalable particles < 10um
• PM2.5= fine particles
• Ultrafine= <0.1um (may be more correlated with disease, but not currently regulated)
• Size doesn't reflect content

Sources of Air Pollution

• Classic:  mobile sources ie cars, trucks etc (high CO2); geographically fixed sources ie power and chemical plants (high SO2)
• Industrial pollutants linked to asthma ie soybean dust in dock areas

EPA Air Quality Index

• Based on criteria pollutants except lead
• Level of 100 is "Standard"
• If all combined < 100 moderate or less concern
• If >100 increasing adverse effect.
• Health alert 200-300

Smog

Smoke + Fog

• Volatile organic compounds +Nitric oxide interacts with sunlight to form ground level ozone
• Major Source: combustion engines/auto exhaust (NO2)
• 90% of smog is ozone in most urban areas
• Ozone peaks in afternoons on warm , sunny days

Outdoor Air Pollution

• OAP in pts living near highways associated in many studies w greater asthma, cough, wheeze in children
• High OAP associated  w short term increase in infant death 1-12 mo of age
• High OAP associated  with increase adult mortality from heart and lung disease

Nitrogen Dioxide

Associations with respiratory effects

• Mean increase in NO2 exposure during childhood associated with decrease in lung growth by puberty
• Strong assoc with acute and chronic lung fxn changes
• Associated with enhanced airway inflammation
• Increases airway response to Ag in asthma
• Increases LPR to Ag challenge

Sufur Dioxide Effects

• Increased exposure linked to ED visits for respiratory illness
• Immediate (within minutes of exposure) effects
• +Tachyphylaxis
• Nasal breathing protective

Ozone

Exposure effects

• Clear association between exposure and asthma exacerbations
• 24-28 hour lag to increased hosp admissions
• Chronic exposure linked to new onset asthma in men, but not women
• Lab challenge: decreased FVC and FEV1; PMN inflamm within 1 hour with up to 24 hour duration

Diesel Exhaust Particle

• Elemental carbon core, but a lot of chemicals cling to surface, therefore total amount of respirable chemical exposure is quite high
• High level exposure assoc with high IgE 
• Exposure skews immune response to TH2

DEP Effects 

• Healthy subjects: incr airway inflamm cells (PMN, Bcells and Tcells, mast cells), cytokines IL6, 8 and 13, incr ICAM and VCAM adhesion molecules
• Mild asthma:  similar and incr methachline response

Indoor Air Pollution

• Primary source: biomass burning ie tobacco, heating sources, attached garages
• Indoor VOC exposure, esp to benzene (dry cleaning and tobacco) assoc w asthma increase  (traps inside, greate than outside)
• Increase in nocturnal asthma:  gas stove, indoor tobacco, fire in fireplace

Tobacco Smoke

• Mainstream (direct to smoker) vs Side Stream (from burning end)
• Nicotine is significant component:  metabolized to cotinine (measurable in saliva,blood, urine, hair)
• Particulates, endotoxin
• Assoc with lung inflammation

Infants of mothers who smoke:

• Lower birth weight
• Lungs smaller
• GSTM1 (enzyme) NULL genotype assoc with early onset asthma, persistent asthma and incr ED visits

"I only smoke outside"

• no signif difference in cotinine levels in infant's hair compared to those of mother who smoked inside

Oxidative Stress and Asthma

Asthmatics:

• decreased antioxidants
• multiple oxidative stessors
• Possible influence of antioxidant response genes ie
• NQO1, GSTM1, GSTP1  (lack of genes related to decreased lung growth)