AIR QUALITY INDICATORS

The EPA uses six "criteria pollutants" as indicators of air quality and has

set standards for each of these under the NAAQS. When an area does not

meet these standards, it is designated as a nonattainment area and must

develop and implement a plan for attainment. The six criteria pollutants

are ozone, carbon monoxide, sulfur dioxide, nitrogen dioxide, particulate

matter, and lead.

OZONE

Ozone, an odorless, colorless gas, made up of three atoms of oxygen, is

the major component in smog. There is "good" ozone and "bad" ozone

depending on its location. The "good" ozone is in the upper atmosphere

and provides a shield from harmful ultraviolet radiation. 
(This ozone shield is being seriously threatened 
by various global warming processes.) 
The "bad" ozone is at ground level where it poses a significant threat to human

health by damaging lung tissue, reducing lung function, and sensitizing

the lung to other irritants, causing a range of symptoms including coughing,

sneezing, pulmonary congestion, and chest pain.

Ozone is created by a complex set of Volitile Organic compounds (VOCs)

and oxides of nitrogen in the presence of sunlight. These chemical reactions

are affected by sunlight and heat, resulting in greater production of

ozone in warmer seasons. Volatile organic compounds are emitted by a

wide range of polluting sources, including dry cleaners, cars, chemical

manufacturers, paint shops, and many others.

CARBON MONOXIDE

Carbon monoxide is a colorless, odorless, and poisonous gas produced

during the burning of fossil fuels (coal and oil). The vast majority of carbon

monoxide is produced by automobiles. However, incinerators, woodburning

stoves, and other industrial sources also contribute. Carbon

monoxide binds with human hemoglobin in a way that precludes the binding

of oxygen. This results in anoxia. The most sensitive populations to

carbon monoxide poisoning are people with cardiovascular diseases and

chronic obstructive pulmonary disease (COPD) and smokers. There is some

evidence that carbon monoxide exposure may actually accelerate atherosclerosis.

Flu-like symptoms such as headache and fatigue are associated

with low-level exposures. Neurologic manifestations include changes in

auditory and visual perception, psychomotor function, and dexterity.

SULFUR DIOXIDE

Sulfur dioxide is a gas that is formed during the combustion of fossil fuels,

during an array of industrial processes, and during the production of energy

from coal, oil, and biomass. It is a major contributor to acid rain. Sulfur

dioxide is also associated with a constellation of health effects, including

respiratory illness, alterations in pulmonary function, aggravation of existing

cardiovascular diseases, and exacerbations in asthma.

AIR QUALITY THREATS

In agricultural areas, where aerial pesticide applications are made, pesticides

may drift, volatilize, and disperse downwind. Ground water, surface

water, soil, and food may become contaminated. The indoor air is also

likely to become contaminated with the pesticide drift. General population

exposure has been well documented, with residues of pesticides and

metabolites found in blood, urine, breast milk, fat tissue, and other tissues.

Health practitioners should factor such potential exposures into their patient

and community assessments.

Incinerators pose a threat to air quality, releasing a range of pollutants

depending on the waste stream composition. They will typically include

the metals (mercury, lead, arsenic, cadmium, chromium, manganese, nickel,

antimony, selenium, zinc, and vanadium); PCBs, furans, polycyclic aromatic

hydrocarbons, and acid gases and oxides of nitrogen, sulfur, and carbon.

Proximity to incinerators is associated with increased local soil lead levels.

A particular concern arising from our poor air quality is global warming,

a change in our global climate resulting from the changes in industrial

and agricultural processes that, in turn, have changed the gases in our

atmosphere. So-called greenhouse gases are those gases (both naturally

occurring and man-made) that are capable of adsorbing heat in the atmosphere.

The naturally occurring greenhouse gases are water vapor, carbon

dioxide, methane, nitrous oxide, and ozone. Man-made contributions to

these gases include carbon dioxide, methane, nitrous oxide, and several

very powerful greenhouse gases: hydrofluorocarbons (MFCs), perfluorocarbons

(PFCs), and sulfur hexafluoride (SF6), which are generated by

industrial processes.

The resulting climate changes occurring from the extraordinary addition

of man-made, greenhouse gases are rising temperatures (.5-1 degree

since the nineteenth century) and a rise in the sea level (4-8 inches in the

last century). Alterations in forests, crop yield, and water supplies are predicted.

There is nothing that will reverse this trajectory in the near future,

and only a global strategy will succeed in addressing the long-term trends.

Because of the inevitability of the warming processes and the potential

public health ramifications of global warming, health professionals should

be educating themselves and weighing in on this very important issue.

Air Pollution

BACKGROUND

In the 1960s, there were a number of visible signs that pollution urgently

needed to be addressed. One of these signs was the brown air that was

engulfing so many of our nation's cities. In 1970, the Environmental

Protection Agency (EPA) was established and significant amendments to

the 1963 Clean Air Act (CAA) were made, setting the stage for a new era

of "command and control" policies to try to turn the tide on what was the

increasingly threatened state of our air. The policies that have been developed

over the years have attempted to address air pollution in a comprehensive

manner by reducing air pollutants from their many sources: mobile

sources (automobiles and trucks), fixed site facilities (factories, waste treatment

facilities, power plants), and through consumer products such as

refrigerants in refrigerators, aerosol spray cans, and other products that

threaten air quality. We are also developing a better understanding of the

association between poor air quality and human and ecological health.

The results of the CAA are noted in some improvements in air quality,

although these improvements are neither uniform for all forms of air pollution

nor consistent globally. Ground-level ozone continues to persist at

unhealthy levels in many areas, as do sulfur dioxide and mercury from

coal-fired power plants. Sulfur dioxide continues to be a major contributor

to acid rain. Although visibility has improved over many U.S. cities, it

is worsening in many third world cities. Airborne persistent organic pollutants

(POPs) are not deterred by national boundaries and are carried and

deposited based on dominant weather patterns.

The CAA required that a set of standards be created that would protect

sensitive populations, such as people who suffer with asthma. These health- based standards are the National Ambient Air Quality Standards (NAAQS).

In 1996, 46 million Americans still lived in areas where the air did not

meet the NAAQS, evidence of our need for continued air quality vigilance.

When the CAA was amended in 1990, Congress additionally mandated

the EPA to regulate "hazardous air pollutants" (HAPs) or air toxics, those

chemicals known or suspected to cause serious health problems. The

amendments named 189 toxic air pollutants for which standards must be

created, many of which are carcinogens, mutagens, and/or reproductive

toxins, including beryllium, mercury, asbestos, vinyl chloride benzene,

arsenic, and radionuclides. Such toxic air pollutants may be gases, metals

and other fine particles, and gases absorbed onto fine particles. Congress

also tightened controls on contributors to acid rain, increased measures for

controlling airborne carcinogens, created cleanup schedules for cities that

were not complying with the NAAQS, and tightened standards for auto

emissions.

 Air pollution sources are described by the location from which they

emanate and by the patterns of their releases. Point source refers to a specific

location such as a smoke stack. Area sources refer to pollutants that

come from a range of smaller generators such as dry cleaners (perchlorethylene),

automobiles, gas stations (benzene), and wood stoves.

Routine releases occur "continuously," certain production activities cause

the release of intermittent emissions known as "batches," and "accidental"

releases occur during explosions, equipment failure, or transportation

accidents. Traffic-related pollution may be referred to as a mobile source!

Pharmacotherapy

Nicotine is an extremely addictive substance, acting on the hypothalamic

center, which controls arousal, concentration, and stress reduction. Nicotine

releases dopamine and norepinephrine, resulting in increased energy and

euphoria, improved concentration, improved hand-eye coordination, and

anorexia. A true drug dependence develops and physiologic withdrawal

occurs after the patient stops using nicotine. Psychological dependence is

also likely to occur, with cravings to start using tobacco again. Nicotine

withdrawal symptoms are more likely if the patient smokes more than 10

cigarettes per day. "Nicotine withdrawal syndrome" is characterized by at

least five of the following within 24 hours: (1) dysmorphic or depressed

mood; (2) insomnia; (3) irritability, frustration or anger; (4) anxiety, restlessness,

or impatience; (5) difficulty concentrating; (6) decreased heart

rate; (7) increased appetite or weight gain.

Because of the addictive properties of nicotine, all patients willing to

quit should also be offered pharmacotherapy unless there is a contraindication.

Medications increase smoking cessation rates and reduce withdrawal

symptoms. The first-line pharmacotherapies recommended are

sustained-release bupropion hydrochloride, nicotine gum, nicotine inhaler,

nicotine nasal spray, and the nicotine patch. The choice of a first-line medication

is determined by the clinician's familiarity with the medication,

the patient's previous experience with the medication, specific contraindications,

and patient characteristics (such as history of depression or

concern about weight gain). Second-line therapies, such as clonidine

hydrochloride and nortriptyline hydrochloride, are suggested when patients

are unable to use first-line therapies because of contraindications or when

first-line therapies fail. A summary of recommended medications is listed

as follows:

First-line medications

.• Nicotine replacement therapy (NRT): Smokers should quit smoking

entirely before beginning nicotine replacement and should not resume

smoking during therapy.

• Transdermal nicotine patch: Several different transdermal patches are

available, and all have lower doses used during tapering. Full-dose

patches are recommended for most smokers for the first 1-3 months,

followed by 1-2 tapering doses for 2-4 weeks each. The main side effect

is local irritation. The patch is preferred by many clinicians because of

ease of instruction in use and fewer compliance problems compared to

nicotine gum.

• Nicotine gum: 2- and 4-mg gum is available over the counter. Users

should not chew too rapidly, chewing for 20-30 minutes per piece.

Instruction in use requires considerable education. Side effects are primarily

local and include jaw fatigue, sore mouth and throat, upset stomach,

and hiccups.

• Nicotine nasal spray: Patients administer one spray per nostril when

they feel the urge to smoke. Because the resulting blood nicotine level

is higher than that produced by the patch or gum, it may be more effeclive than other NRT delivery systems in highly addicted smokers. Side

effects are irritation of the nose causing burning, sneezing, and watery

eyes; tolerance to these effects usually develops in 1-2 days.

• Nicotine vapor inhaler: The inhaler is marketed in a cigarette-like plastic

device and has a unique role because it fulfills the "hand-mouth"

behavior of smoking. It can be used as frequently as desired. Nearly 80

puffs are required to achieve nicotine doses equivalent to a cigarette.

• Bupropion: Smokers are more likely than nonsmokers to have a history

of major depression; nicotine may act as an antidepressant in some

smokers. Bupropion, an antidepressant, is effective in some smokers. It

is dosed at 150-300 mg per day for 7 days before quitting, then at 300

mg per day for the next 6-12 weeks. Bupropion can also be used in conjunction

with a nicotine patch. In excessive doses, bupropion can cause

seizures and should not be used in patients with a history of seizures or

eating disorders.

Second-line medications

• Clonidine

• Nortriptyline

Environmental Tobacco Smoke and Smoking Cessation

DEFINITION AND HEALTH EFFECTS

Environmental tobacco smoke consists of "mainstream" smoke exhaled

by an active smoker, and "sidestream" smoke released from the smoldering

end of a cigarette, pipe or cigar. ETS contains more than 3,800 different

chemicals. ETS is qualitatively similar to mainstream smoke, but

contains higher quantities of certain toxins such as ammonia, formaldehyde,

and nitrosamines. It is the main source of particulate matter of less

than 2.5 microns, a size that reaches the lower airways.

In 1998, more than 47.2 million U.S. adults, 24% of the population,

were cigarette smokers (Centers for Disease Control and Prevention, 2000).

Forty-three percent of children aged 2 months to 11 years lived in a home

with a cigarette smoker (Pirkle, Flegal, Bernert, et al., 1996). Young children

may spend a significant amount of their time indoors, in their own

homes, relatives* homes, and child care settings, exposing them to ETS

and making them passive smokers.

EFFECTS ON ADULTS

Adults may be exposed to ETS through a tobacco-using spouse or housemate.

ETS has been classified as a group A human carcinogen, indicating

that there is sufficient scientific evidence supporting a causal relationship

between exposure to ETS and the development of cancer. The U.S.

Environmental Protection Agency has estimated that ETS is responsible

for approximately 3,000 lung cancer deaths per year in nonsmokers in the

United States. In addition, exposure to ETS has been linked with an

increased risk of developing myocardial infarction, reduced pulmonary

function, cough, headache, nasal congestion, and eye irritation.

EFFECTS ON CHILDREN

Children exposed to ETS through maternal smoking may show a number

of negative health effects (American Academy of Pediatrics, 1999) including

(1) Lower respiratory tract infections: These infants are 38% more

likely to be hospitalized for pneumonia in the first year of life than children

whose mothers do not smoke; when both parents smoke, the infants

are twice as likely to be hospitalized than children whose parents do not

smoke. (2) Middle ear effusions: Children of parents who smoke are more

likely to develop middle ear effusion and otitis media. (3) Asthma: These

children are more likely to develop asthma, and those with asthma may

have more severe symptoms and more frequent exacerbations. (4) Sudden

infant death syndrome (SIDS): A growing body of evidence links ETS

exposure to an increased incidence of SIDS, independent of gestational

age or birth weight.

Exposure to ETS before age 10 raises the risk of developing leukemia

and lymphoma in adulthood.