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 smog, O3, aerosol oxidizing atmosphere photochemical smog Formation of NO x 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

org O2

photochemical smog “an ozone layer in the wrong place”

Get second stage process in the atmosphere 2 NO + O2 2 NO2 Slow process Genesis of Smog NO2 + hv NO + O λ < 0.4µ O + O2 + M O3 + M O3 + NO NO2 + O2 To this, one add the organic molecules

fast kinetics

Role of Hydrocarbons 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

from NO2 + light

O O // // R′ - C + NO2 R – C \ \ O – O 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 O3 threshold 0.02 ppm very noticeable 0.2 ppm 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, Anthropogenic ~ 30% ~ 70% degradation of Internal combustion engine chlorophyll (~60%) Forest fires, aircraft (21%) garbage incineration (8%) industry (11%)

Sinks a) CO CO2 (lower stratosphere)

(CO + OH CO2 + H) b) biological removal in soil Levels “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

SO 2 rxns in the atmosphere SO2 in atmosphere short lives (hrs or days) Principal fate is oxidation to SO3 catalytic (water droplet + metal salt or NH3) SO2 night – high hum. SO4 photochemical SO3 day – low hum. SO2* SO3 SO3 + H2O H2SO4 (NH4)2SO4

Lifetimes of Atmospheric S cpds H2S < 1 day (conversion to SO2 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

O2

NH3

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 bio. decay) HNO3

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 rural 50% auto 50% industry heavily industrialize area

NO x in Urban Atmosphere NOx NO, NO2 Photochemical Cycle NO2 + hv NO + O O + O2 + M O3 + M O 3 + NO NO 2 + O 2 O3 + NO2 NO3 + O2 high conc. Overall cycling

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

% Death

50

100

log Dose

LD50

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} CO2 + CH4 Other biogenic hydrocarbons: ethylene • reactions (alkanes) OH radical attack CxH2x+1 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

bact.

O2

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 + HO2H-C-OH

C H

electron delocalized

O2

OH

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 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 (fire extinguishers) CBrF3

Clx

Concern with CFCs is their stability (do not biodegrade), large production, ozone depletion Cl2CF2 Cl + ClCF2 Cl + O3 ClO + O2 ClO + O Cl + O2 or ClO + NO Cl + NO2 Cl + O3 ClO + O2 Cl + O3 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)

hv

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 most prevalent in contin. aerosols 10 – 20 % of mass 0.1 < R < 1 µ Large particles | scatter vis. light R > 1 µ Giant Sedimentation Stokes Law v = gd2 (p 1 – p 2) p density – p1 particle; p2 air 18η 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