Download Photochemical Smog brownish haze, plant damage, eye irritation

Photochemical Smog
brownish haze, plant damage, eye irritation, respiratory
problems
ingredients
sunlight
NOx
meteorological condition that allows rxn before
dispersal
volatile organic cpds (hydrocarbons)
sunlight + NOx org
smog, O3, aerosol
O
2
photochemical smog
“an ozone layer in the
wrong place”
oxidizing atmosphere
photochemical smog
Formation of NOx
oxidation of N2 at high T
N2 + O2 2 NO
primary mechanism
N + O2
NO + O
O + N2
NO + N
Sources
motor vehicles
fossil fuel power plants
Control of NOx must focus on lowering combustion T
(a) exhaust gas recirculation
(b) increase fuel/air mix (increase hydrocarbons)
(c) reduction catalyst
Atmospheric oxidation of NO
After combustion, mostly NO
< 2% NO2 auto
< 10% NO2 power plants
Get second stage process in the atmosphere
2 NO + O2
2 NO2
Slow process
Genesis of Smog
NO2 + hv
NO + O
O + O2 + M
O3 + M
O3 + NO
NO2 + O2
fast
kinetics
To this, one add the organic molecules
λ < 0.4µ
Role of Hydrocarbons
from NO2 + light
First step
R+O
R′O + R″
Example
H
H
H
\
/
|
C=C +O
H–C–C–O
/
\
| |
H
H
H H
Also
R + O3
R′O + …
O
and
||
RCHO + hv
R + HC
A further rxt involved the oxidation of the free radical species
R + O2
ROO
These peroxy radicals can react further
O
//
R′ - C
\
O–O
+ NO2
O
//
R–C
\
O – O – NO2
peroxyacyl nitrate (PAN)
O
//
R′ - C
+ NO2
\
O
Intensity of smog ∝ total axidant concentration
Typical series of reactions for one alkene
Effects of Smog
oxidizing agents
O3, NO2, PANs
plant damage, color air, eye irritation material
measure smog intensity by total oxidant
Eye irritants
¾ of population affected
PANs are most potent
Odor
threshold 0.02 ppm
very noticeable 0.2 ppm
O3
Toxicology
respiratory system
susceptibility to infection
Plant damage
agricultural losses
Reactivity
Emission control must be based on reactivity, not total
amount of hydrocarbons.
Motor Vehicles
auto => CO
organic cpds
NOx
Pb cpds
Hydrocarbon Release
Exhaust 55%
Gas Tank 20%
Blowby 25%
The catalytic converter
reduction chamber (Rh catalyst)
hydrocarbons + H2O
H2 + CO
2 NO + 2 H2
N2 + 2 H2O
oxidation chamber (Pt/Pd catalyst)
2 CO + O2
2 CO2
hydrocarbons + 2 O2
CO2 + 2 H2O
reasonably effective; problem remains for older cars
50% HC, CO ó 10% cars
Reformulated Gasoline
(C2H5)4Pb
PbO, PbO2
terminate HC chain rxns
terminated in US
Canada, Europe: methylcyclopentadienyl manganese
banned in US (?)
tricarbonyl (MNT)
Mn3O4
Mn
US
increase aromatics in gasoline (benzene, toluene, xylene
BTX) not good idea
Use “oxygenated” fuels
CH3OH
C2H5OH
MTBE
methyl + ethyl ethers of t-butyl alcohol
ETBE
Complaints: (MTBE) health complaints
little effect in new cars;
max effect in older cars.
EPA favors ethanol
Oil industry favors MTBE
Gasohol (15% EtOH) is only viable due to farm subsidies
Diesel engines
a) excess air
b) no spark plug – same T as spark-ignited
Poor maintenance => excess particulates / HC
The Los Angeles Basin
Semi permanent inversion layer complicates problem
(~ 75%)
1500
400m elevation
Population > 8 x 106
Non-existent mass transit
single family houses
Large geographic area
Summer, spring west wind
Winter
east wind
Typical episode
Commuter traffic begins 0600
Sun rises
NOx
O
Traffic peak 0800
NOx, HC buildup
O oxidizes them
O3 rises
oxidant levels rise
1000
eye irritation problem
yellow-brown air
O3 smell
respiratory distress starts
PE classes suspended
1200
NOx
PAN
smog front moves east
Recent Progress
Inorganic Pollutant Gases
Mass Balance (CO)
Sources: Natural,
~ 30%
degradation of
chlorophyll
Sinks
a)
Anthropogenic
~ 70%
Internal combustion engine
(~60%)
Forest fires, aircraft (21%)
garbage incineration (8%)
industry (11%)
CO CO2 (lower stratosphere)
Levels
(CO + OH
CO2 + H)
b) biological removal in soil
“background” ~0.1 – 0.2 ppm
city
10 – 20 ppm
residence time ~ 0.1 yr
US std
9 ppm / 8 hr
35 ppm / 1 hr
CO displaces O2 in hemoglobin carboxyhemoglobin
100ppm
easily identified health problems
Atmospheric S Cpds
gases
SO2, H2S
particulate SO4= (H2SO4 or (NH4)2SO4)
Sources
(man made)
(natural)
H2S volcanoes, sulfate aerosols, decomposition of org. mat’l
SO2
H2S + 3/2 O2
SO2 + H2O
Global S Cycle
SO2 rxns in the atmosphere
SO2 in atmosphere short lives (hrs or days)
Principal fate is oxidation to SO 3
catalytic (water droplet + metal salt or NH3)
SO2
night – high hum.
SO4
photochemical
SO3
day – low hum.
SO2* O2 SO3
SO3 + H2O
H2SO4
(NH4)2SO4
NH3
Lifetimes of Atmospheric S cpds
H2S < 1 day (conversion to SO 2 by O, O2, O3)
SO2 < 3 days (diffusion to vegetation, oxidation,
washout)
=
SO4 ~ 1 week
General levels of S cpds
H2S 0.002 – 0.02 ppm
SO2 0.002 – 0.01 ppm
SO4= ~ 2 µg / cm3
Effects of Atmospheric SO 2
Death => 500 ppm
~ 1 ppm problems
Reg Stds
0.6 ppm => warning level
1 hr
0.5 ppm
3 hr
0.5 ppm
24 hr
0.14 ppm
annual average 0.03 ppm
Scrubbers
Sulfate Aerosols
H2SO4
react with NH3 gas in air (NH3
HNO3
bio. decay)
Get A/B chemistry
H2SO4 (aq) + 2 NH3 (s)
(NH4)2SO4 (aq)
Evaporation of H2O leads to solid particles containing
SO4=, HSO4-, NH4+
(NO3- on West Coast)
“Sulfate Aerosols”
lead to visibility reduction / haze 0.4 – 0.8 µm
4 – 9% of mortality rate in US due to sulfate aerosol
Nitrogen Containing Cpds
N2O, NO, NO2, NH3, NO3-, NH4+
N2O “natural” soil
atmospheric rxn
NO/NO2
air pollutants, nat. + manmade
fuel burning (high T)
NO
Global emissions
NOx
auto
50% auto
50% industry
rural
heavily industrialize area
NOx in Urban Atmosphere
NOx
NO, NO2
Photochemical Cycle
NO2 + hv
O + O2 + M
O3 + NO
O3 + NO2
Overall cycling
NO + O
O3 + M
NO2 + O2
NO3 + O2
high conc.
Urban Concentrations
Reg limit 0.05 ppm
Organic Air Pollutants
Toxic Chemicals
1.
Acute vs chronic toxicity
low, prolonged dose, lapse between
exposure + effect
rapid, serious response to high, short-lived dose
LD50; dose-response curves
100
% Death
50
LD50
log Dose
Typical chronic effect
2.
Cancer
uncontrolled cell division, consuming vital tissues
- mutations in cell’s DNA at positions that specify
synthesis of key regulatory proteins
many mutations needed => long latency periods
carcinogens operate in 2 ways:
mutagens – attack DNA bases
promoters – increase cell division (alcohol/liver cancer)
mutagens
- electrophiles – (react with e-rich DNA bases)
mutagen
metabolite (electrophile)
Relation between chemicals and cancer
Smoking ó 30% of US cancer deaths, 25% heart attacks (fatal)
occupational exposure
vinyl chloride liver cancer
benzene
leukemia
asbestos
lung cancer
Ames data
Organic Cpds in Air
6/7 of these cpds are natural in origin
Most prevalent cpd is CH4 (1 ppm in troposphere)
2{CH2O} bact. CO2 + CH4
Other biogenic hydrocarbons:
ethylene
• reactions (alkanes)
OH radical attack
CxH2x+1
O2
CxH2x+1OO
CxH2x+1O
• reactions (alkenes)
hydrogen abstraction to form H2O
or
more likely, addition to =
|
| |
|
|
– C = C – C – + OH
HO – C – C – C –
|
| | |
O
O
| | |
HO – C – C – C –
| | |
H
Aromatics
Terpenes
O2
Causes blue haze (Smokey Mtns)
Typical rxns (O3)
Man made hydrocarbon release
alkanes
alkenes
aromatics
• originate in petroleum pdts
in complete combustion
direct release
concern is with reactive alkenes
Origin:
solvents, gasoline, tobacco smoke
Rxns:
usually unreactive, but OH radical can add to
benzene ring
OH
+ OH
H-C-OH
C
H
electron
delocalized
O2
+ HO2
also get relatively unreactive PAH.
Oxygen Containing Cpds
(alcohols, phenols, ethers, acids)
Alcohols
solvents, used in chemical industry
volatile
free radical rxns, with hydrogen abstraction
Phenols
heavy, industrial use
CH3
Ethers
|
MTBE
CH3 – O – C – CH3
|
gasoline additive
CH3
Aldehydes + Ketones
RCHO
RR′C = O
Origin: a) end pdt of decomposition of peroxylradicals
O
O
O
| | |
| || |
HO – C – C – C –
– C – C – C – + HO
| | |
|
|
O
O
| | |
| | |
HO – C – C – C – H
– C – C – C = O + HO
| | |
| |
H
b) HCHO (formaldehyde)
O
(CH3)2C = O (acetone)
||
CH3CHO + hv
–C–C–H
| *
absorption by C = O
H
|
H – C + HCO
|
H
O
O
||
||
R – C – R′ + hv
R – C + R′
Organohalides RX
of special note
vinyl chloride
pipe, tubing
angiosarcoma
TCE
degreaser, dry cleaning
decaffeination
(regulated)
insecticides, etc
water pollutants
Clx
PCBs
+ Cl2
+ HCl
209 congeneus
Manufactured from 1929 to 1977. Because they are non
degradable, they persist in environment. They bio accumulate.
Effects not easy to establish
occupational => chloracne
chronic problems
CFCs
(Chlorofluorocarbons)
CCl3F (CFC – 11)
C2Cl3F3 (CFC – 113)
CCl2F2 (CFC – 12) C2Cl2F4 (CFC – 114)
related cpds: Halons
CBrClF2
CBrF3
(fire extinguishers)
Concern with CFCs is their stability (do not biodegrade),
large production, ozone depletion
Cl2CF2 hv Cl + ClCF2
Cl + O3
ClO + O2
ClO + O
Cl + O2
or
Cl + O3
ClO + O2
ClO + NO
Cl + O3
Cl + NO2
ClO + O2
PCDD, PCDF
Concern is their toxicity
TCDD
causes birth defects, cancer, skin disorders, liver
damage, suppression of immune system, death
However large variations in toxicity among species
(0.6 – 3000 µg / kg)
Origin
bleaching paper pulp with Cl2
primary source is combustion. Burn Cl – containing
mat’l
dioxin
chlorine need not be organically bound (wood stoves)
primary exposure route for humans in the diet (bioaccumulation)
daily dose ~ 0.1 ng TEQ/day ~ detectable effects in lab animals
Particulate Matter (Aerosols)
Dispersed solid or liquid matter in gaseous medium
d < 100 µm
Misc. facts
Variable sizes + composition
Primary vs secondary pollutants
Anthropogenic vs natural
90% of particulate matter ≡ natural
mean τtroposphere ~ 5 days
Importance
Human Health
Catalyst/site for atmospheric rxns
SO2
Effect on visibility
Sources + Sizes
Aerosol formation mechanisms:
Breakup (dispersion aerosols)
Agglomeration
Breakup
rock crushing
cement manufacturing
coal
weathering
topsoil, sand erosion
volcanic eruptions
sea salt
~ 200 (~0.1 µ) particles formed per bubble
Agglomeration
coagulation of gas molecules to form liq. or solid aerosols
Particle Size
R < 0.1 µ Aitken
0.1 < R < 1 µ
R>1µ
Large
Giant
most prevalent in contin. aerosols
10 – 20 % of mass
particles | scatter vis. light
Sedimentation
Stokes Law
v = gd2 (p1 – p2)
18η
p density – p1 particle; p2 air
η ≡ fluid viscosity (air viscosity)
= 170 x 10-6 g/cmsec
g = 981 cm/sec2
Result
Large particles are of less concern because they fall out
quickly, they are not respirable, small relative surface area for
pollutant transport, efficiently removed.
TSP not so relevant; refer to PM10
Size Distribution
f (r, r +dr) = CR-(βH) ∆R
β ≈ 3.
Chemical Processions for Particle Formation
Combustion (high T)
small dia. particles
metal oxides
organics
PAH hydrocarbons
benzo (a) pyrene
Source Strengths
Effect of Particulate Matter
Visibility
Health