In general, criteria pollutants have a known threshold dose, below which noadverse health effects are known to remain after cessation of exposure.. Human health effects data are readily
Trang 1And what may be the cause of these troublesome effects, but the inspiration of this infernal vapour, accompaning the Aer, which … enters by several branches into the very Parenchyma, and substance of the Lungs, violating, in this passage, the Larynx and Epiglottis, … which, becoming rough and drye, can neither be contracted, or dilated for the due modulation of the Voyce.
Fumifugium, 1661
The effects noted during the 1952 London Smog Disaster were obvious but notperceived — nearly 1000 deaths per day, where beforehand the normal death ratewas a few hundred deaths a day at most It was reported that the increase of deathsduring the London smog siege was not noticed during the event, but the shortage
of coffins and flowers was Today we are much more aware of acute as well as term or chronic health effects
long-Air pollution was known to cause damage to the entire ecosystem even before
Fumifugium was published Such damage includes adverse effects on human health;damage to crops, vegetation, and forests; and finally, damage to materials that weall use
Our goal in this chapter is to review and evaluate the effects on human health
of the different air contaminants Then, we consider contaminants’ effects on etation, crops, and finally, other materials
veg-TIME EFFECTS AND SENSITIVITIES
A CUTE VERSUS C HRONIC
As seen during the London Smog Disaster, the immediate effect of the air pollutionwas acute — death Only in the last few years has there been new research to showthe long-term complications of air pollution that occurred months and years earlier.Initial estimates were that about 4,000 people had died as a result of the smog siege;now the epidemiological evidence indicates that about 12,000 died of complicationsover the course of 6 months following that event
There are two time-related categories of health effects The first deals with acuteeffects, that is, those health effects that tend to act immediately on a specific targetorgan or point of entry into the human body In the air pollution field, these points
of entry are typically the eyes and the lungs, as they are in immediate contact withthe ambient air Burns and asphyxiation are other examples of acute health effects
It is possible for a contaminant to have an acute effect that is different from itschronic effect
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Chronic (Greek, chronos) effects are those that refer to time functions of exposure.Thus, there may be long-term exposure or a long period between an exposure andthe effect In general, this latter term refers to a more specific concept, termed latency
S ENSITIVE P OPULATIONS
The general population ranges from vigorously hearty individuals to those who areparticularly susceptible to ambient pollutants Table 2.1 lists those general populationgroupings that are considered sensitive to air pollution In the London Smog Disaster,
it was initially thought that only the elderly were affected However, later researchhas shown that most of the deaths occurred in the 45–65-year-old age category.Within each of these general population groupings there may be some overlap
of effects as well as the possibility of multiple sensitivities Pregnancy is anotherconsideration It has been estimated that roughly 7% of the population already suffersfrom some forms of cardiovascular disease, with approximately 9% being susceptible
to chronic respiratory diseases Ten percent may be considered elderly, with possibly20% being children under the age of 14 years On the average, perhaps an additional7% of the general population may be involved in some form of vigorous athleticactivity Again, although not exclusive, these numbers would indicate that perhaps halfthe total population in any location may have an existing sensitivity to air pollution
CRITERIA VERSUS NONCRITERIA AIR POLLUTANTS
There are differences between how criteria and noncriteria pollutants act Beforeevaluating specific pollutant effects, it is instructive to differentiate between thesetwo groupings of air pollutants; Table 2.2 summarizes the differences Lead, a criteriapollutant, is the exception to this discussion, as it is obviously toxic
In general, criteria pollutants have a known threshold dose, below which noadverse health effects are known to remain after cessation of exposure With respect
to carcinogens, there is no known threshold to which we can point with confidence
In comparison to the noncriteria or hazardous air pollutants (HAPs), which arepotentially numerous, there are only six criteria air pollutants Other significantdifferences are that the gaseous criteria pollutants occur in the ambient air at thelevel of parts per million, whereas HAPs tend to reach the level of parts per billion
TABLE 2.1 Population Groups Sensitive to Air Pollution Population Group Percentage of Population
Cardiovascular disease 7 Chronic respiratory disease 8.9 Elderly (>65 years of age) 9.6 Children (<14 years of age) 20
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Indeed, it has only been with the advent of modern technology that we have beenable to regularly and routinely monitor these trace contaminants in the ambient air.The criteria pollutants are not bioaccumulated in tissues, whereas many HAPs
do tend to bioaccumulate Thus, HAPs may have significant effects on long-termhealth
The lung is the primary target organ for criteria pollutants (with the exception
of carbon monoxide) The noncriteria or hazardous air pollutants, in contrast, havepotentially many target organs
Human health effects data are readily available for the criteria pollutants becausethey have been studied not only in the ambient air (in some cases for over 100 years)but also in occupational exposures With respect to the HAPs there is much lesshuman health data available, particularly for dose–response relationships for carcin-ogens, mutagens, and teratogens The effects of the criteria pollutants tend to last aperiod of minutes to months, whereas the HAPs tend to have long-term effects.Finally, the criteria pollutants exhibit more immediate or acute effects; HAPstend to cause chronic health effects
C RITERIA A IR P OLLUTANT E FFECTS
Of the criteria pollutants, ozone, sulfur dioxide, fine particulates, and nitrogendioxide have both acute and chronic health effects Carbon monoxide has acuteeffects only, whereas lead, being a toxic metal, has chronic effects (at ambient airlevels)
Ozone
Ozone is a strong oxidizer that affects the respiratory system, leading to damage oflung tissues Among the acute effects are cough and chest pain, eye irritation,headaches, lung function losses, and asthma attacks
Within the lung itself, there is damage to the ciliated cells These cells areresponsible for the clearance mechanism for particulate matter in the lungs
Figure 2.1a shows healthy lung tissue with active cilia, and Figure 2.1b shows lung
TABLE 2.2
Criteria and Hazardous Air Pollutant Comparisons
Criteria Pollutants* Hazardous Air Pollutants
Not bioaccumulated Some may bioaccumulate
Lung is primary target organ (except CO) Many target organs
Human health effects readily available Human dose–response data rarely available Effects generally occur in from minutes to months Effects generally occur after long latent
period (years) Primarily acute effects Primarily chronic effects
* As regulated under the Clean Air Act, except lead.
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tissue after exposure to ozone for an extended period of time The damage to thecilia is apparent
In addition, ozone damages the alveoli cell membranes These membranes arethe individual air sacs in the lung in which the exchange of oxygen and carbondioxide takes place between the air and the blood
Chronic exposures to elevated ozone levels are responsible for losses in immunesystem functions, accelerated aging, and increased susceptibility to other infections
In addition, because of its nature as an oxidizer, there are prospects for permanentloss of the alveoli cells
Sulfur Dioxide
Sulfur dioxide has its own acute health effects, again with the lungs being the targetorgans These adverse health effects include irritation and restriction of air passages
FIGURE 2.1a Healthy lung tissue with active cilia.
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There is reduced mucus clearance from the restricted air passages and chest tightness
Figure 2.2 shows, in an e-ray of the lung, the differences before and after exposure
to sulfur dioxide Under normal conditions, the lung passages are open; after sure, the lung passages constrict in a response to SO2 This constriction also furtheraggravates other health conditions
expo-Otherwise healthy individuals may also experience sore throats, coughing, andbreathing difficulties, in addition to a noticeable odor at concentrations approaching0.5 ppm There are some indications of an increased sensitivity to sunlight resultingfrom acute exposures
For chronic effects, sulfur dioxide is responsible for immune system suppressionand for an increased probability of bronchitis The latter is of particular concern forindividuals with emphysema There are some indications that chronic exposure tosulfur dioxide may also act as a cancer promoter in addition to being an immunesystem suppressor
FIGURE 2.1b Lung tissue with damage to cilia after exposure to ozone for an extended period of time.
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Particulate Matter
Among the acute health effects of elevated concentrations of fine particulates areincreases in mortality rate, increased incidence of asthma and bronchitis, andincreased rates of infection in the respiratory system These particulates also directlyirritate the respiratory tract, constrict airways, and interfere with the mucus lining
of the lung passages
Among the chronic effects of fine particulates are losses of lung capacity andlung damage, resulting from scarring caused when fine particulates are not clearedfrom the lung passages or alveoli In addition, fine particulates act as carriers fortoxic contaminants and, in particular, heavy metals This occurs when the contam-inants exist in a fume or a vapor state and condense onto the fine particulates Inthe alveolar regions, heavy metals may be absorbed into the blood and circulated toother parts of the body
Particulates, and in particular the fine-particulate fractions, are also responsiblefor visibility reduction Visibility loss may be considered a psychological stress
Nitrogen Dioxide
In addition to participating in the formation of photochemical ozone at ground level,nitrogen dioxide has its own particular health effects The acute effects of nitrogendioxide are both direct and indirect The direct effects are damages to the cellmembranes in the lung tissues as well as constriction of the airway passages.Asthmatics are, in particular, affected by these acute effects The indirect effects arethat nitrogen dioxide causes edema, or a filling of the intercellular spaces with fluid,which may develop into local areas of infection
FIGURE 2.2 The lung after (left) and before (right) exposure to sulfur dioxide.
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Among the chronic effects of long-term exposures to nitrogen dioxide is necrosis,
a term for direct cell death In addition, there is evidence that NO2 causes a thickening
of the alveolar walls of the lungs, which interferes with efficient oxygen and carbondioxide exchange across those cell walls There also appears to be a correlation withincreased susceptibility to other lung diseases through chronic exposures
Some evidence indicates that when mice are exposed to nitrogen dioxide andinjected with cancer cells, they develop more cancerous lung nodules than do micewho are injected with cancer cells but who breathe clean, filtered air Other studies
of NO2 exposure on mice indicate that changes in lung tissue structure are similar
to those that occur in human lungs in the early stages of emphysema There alsoappears to be evidence that other target organs may be affected by nitrogen dioxide.The University of Southern California conducted experiments demonstrating thatinhaling NO2 enlarges the spleen and lymph nodes in mice The spleen and lymphnodes are important organs in the body’s defense system This finding indicates thatthe body’s immune system may be adversely affected by exposure to chronic levels
The concerns about carbon monoxide are even greater at higher elevations, wherethe partial pressure of oxygen is lower and where many persons may already sufferfrom an inadequate oxygen supply
Lead
Lead, being a toxic metal, acts in a different manner than the other criteria pollutants
It is a systemic toxicant and therefore damages a number of different target organs
in the body Because it is a metal, it is distributed throughout the body and can beresponsible for central nervous system damage Brain functions affected includebehavioral changes, losses of muscle control and learning difficulties These are themost important aspects of lead exposures
In addition, lead impacts certain key enzymes in the production of red bloodcells, which brings on anemia This is the most characteristic symptom of leadexposure in both children and adults In addition, there is evidence of kidney damage,liver and heart damage, and damage to the reproductive organs A combination ofeffects, including damage to enzyme systems, is possible in these target organs 7099_book.fm Page 27 Friday, July 14, 2006 3:13 PM
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BASIC PRINCIPLES OF TOXICOLOGY
A basic understanding of the elements of toxicology is important to understand airpollution health effects The majority of this information deals with animal studies.Similarities and differences, of course, are drawn to epidemiology studies and totrue human exposures in laboratory settings
S OURCES OF H EALTH E FFECTS I NFORMATION
What we know about the effects of air pollution on people comes to us from threemajor sources Each of these sources is needed to gain a good understanding of airpollution’s health effects These three sources are animal studies, human exposurestudies, and epidemiology
Animal effect studies are used to a large extent because we can control theconditions surrounding the animals The animals used range from microbes to mice
We are also able to perform long-term (potentially generational) studies on testanimals This is a positive aspect because we are able to monitor and controlconditions Unfortunately, as a result of species differences noted later, the healtheffects for a given exposure to an air pollutant are not necessarily transferable tohuman beings
The second technique is to gather effects data by human exposure studies Thesestudies are performed under controlled conditions in a laboratory, using exposures
of specific contaminants to real people; therefore, the results are directly transferable
to different segments of the population In one sense, this may provide us with thebest data, as it is species specific Such exposure studies are limited, however,because we cannot expose individuals to cancer-causing agents or to those that causereproductive toxicity or other life-threatening contaminants These studies are expen-sive and are generally limited to a maximum period of 8 hours Therefore, no chroniceffects may be studied Likewise, we are not able to gain an understanding of subtle,
or microcellular, effects that may occur through human exposure to various aircontaminants
Epidemiology is another approach by which we are able to study humanresponses to air contaminants This type of study may be done over long time periods.Thus, the data may allow for evaluations of chronic exposures Also, we are dealingwith real people The limitations are that the researchers have a very limited controlover significant variables involved, such as lifestyle, smoking habits, age, sleeppatterns, nutrition, and so on These studies also tend to be costly because a greatdeal of time must be spent observing individuals and accessing medical records over
a period of years
It is important not to assume only one source of exposure when dealing withhealth data Early assumptions made about air pollution and lead-based paint beingthe only sources of lead exposure in Southern California were recently found to beerroneous It was discovered in 2004 that children with high blood lead levels wereeating certain flavored candies from Mexico that were found to be significant sources
of lead poisoning Between 5% and 10% of all the candy tested was found to beover the federal regulatory lead level
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D OSE –R ESPONSE
Toxicity tests, and what we learn from them, are at the heart of understanding healtheffects Because it is illegal to expose people to suspected toxicants, other speciesare used to quantify the effects that may be expected from exposure to hazardous
or toxic substances
A generalized dose–response curve is seen in Figure 2.3, which illustrates theresponse of test animals to a chemical From this dose–response curve, one maydetermine the LD50 for those animals to that chemical (LD50 is the lethal dose for50% of the test animals.) Of particular importance is the shape of the curve and theimplications thereof First, it is an S-shaped curve, which indicates that effects aredifferent for incremental changes in dose Second, it does not go through the origin(zero response at zero dose) This indicates that the true effect at very low doses isunknown (or zero for some minimal dose) These important points are examined indetail later
For the lower dashed line in the figure, one may see that there is essentially noresponse until some low-level dose is reached, at which point the effect becomestruly observable This is the threshold concept and is observed for virtually allmaterials The upper dashed line is a linear extrapolation between the lower testpoints and the origin on the curve This extrapolation presumes that there will always
be a response for a given dose All other extrapolations are based on assumptions
on the part of the investigator
Major species differences do exist, and they present the biggest problem in trying
to extrapolate dose–response information to all dosage levels Absorption rates,metabolic activity, and excretion rates are all included in the differences betweenspecies Individual differences in the same species can have a dramatic effect on theresponse of the test animal Habitat (e.g., aquatic vs terrestrial) is also important,and such features as genetic traits, sex and hormones, nutrition, and age of the testanimals in some degree also give a scatter in the response data to a given dose Aftermicrobes, mice and rats are used This is because they are cheap, have a relativelyshort life span, and are mammals
FIGURE 2.3 Generalized dose–response curve showing low dose extrapolations.
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The four most important parameters in comparing dose–response curves andattempting to draw conclusions are species, dose, time period, and endpoint orresponse chosen The biggest problems in interpretation are related to interspeciesdifferences in response to any given chemical
ROUTES OF EXPOSURE
The four major routes of exposure to hazardous chemicals are inhalation, ingestion,dermal absorption, and injection Within the environmental field, the last is a minorroute of exposure to environmental contaminants compared with the other three.Because injection is most often used with experimental animals, the results ofexperiments using animal tests may not be comparable with the effects from otherroutes of exposure
I NHALATION
Inhalation, the major route of entry involved when dealing with air pollutants,involves the intake of airborne chemicals during breathing The solubility of thematerial in the blood affects the degree of its absorption Once in the blood via thelungs, it goes directly to the brain and the rest of the body
The most common example of environmental exposure via inhalation is theabsorption of carbon monoxide through smoking Carbon monoxide has severalhundred times greater binding affinity for hemoglobin than oxygen does Hemoglo-bin is the iron-based organic compound that is responsible for all oxygen transport
in the blood Oxygen is “bound” by hemoglobin and is later given up by hemoglobin
to the tissues When oxygen is displaced irreversibly by carbon monoxide, thetransport phenomenon is not able to function, and oxygen starvation of cells begins.The retention of airborne particulates that are, or that may carry, toxic elements
or chemicals is highly dependent on particle size because of the structure of thehuman lung The smaller sizes penetrate deeper and have a greater effect
RESPONSE TO AIRBORNE CHEMICALS
Chemical agents have a different effect on different member organs of the bodydepending on the dose and route of exposure Chemicals target specific organsdepending on oil or fat solubility, the effect that the chemical may have on enzymeactivity, or physical interruption of the transmission of electrical impulses
Table 2.3 lists a variety of systemic poisons that influence different target organs
in the human body by type of chemical or hazardous substance The hepatotoxicagents, such as carbon tetrachloride, primarily affect the liver, whereas nephroticagents (halogenated hydrocarbons) affect the kidneys The neurotoxic agents thataffect the nerve system include methyl alcohol, carbon monoxide, heavy metals, andorganometallic compounds The hematopoietic toxins affect the blood or blood cellsand consist of aromatic compounds such as benzene, phenols, aniline, and toluidine.7099_book.fm Page 30 Friday, July 14, 2006 3:13 PM
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The anesthetic or narcotic chemicals (which affect consciousness) consist of ketones,aliphatic alcohols, and double-bonded or “ether” types of organic compounds
T HE L UNGS
Of all of the body organs, the lungs are the most quickly affected by air contaminants.This is because the lungs are in constant contact with the environment Also, thelungs have a surface area of 70–100 m2, as opposed to the skin, at 2 m2, or theintestinal tract, at about 10 m2 This is an important point because the rates ofabsorption of various contaminants are direct functions of the surface area exposed
to a contaminant Among the criteria pollutants that have a direct and adverse effect
on the lungs are ozone, sulfur dioxide, nitrogen dioxide, and fine particulates
Figure 2.4 presents the various passages and sections of the human lung Thelung acts as a particle filter through its construction As one goes deeper in the lungs,one finds more narrow and torturous paths, which present an aerodynamic obstruc-tion to particle movement Particle size, therefore, determines where particles will
be deposited in various portions of the lung (the smaller, the deeper) Gases penetrate
to the deepest segments of the lung
The nose and pharynx will capture particles from 5 µm to greater than 50 µm
in diameter The area from the larynx down to the bronchi regions of the lungscollects particles from 1 to 5 µm in size The smaller portions of the lungs, thebronchioles and alveoli, will collect particles down to the 0.5 µm range Particlessmaller than 0.05 µm will be exhaled When speaking of particle size, the aero-dynamic particle size is the reference, not the physical particle size
TABLE 2.3 Systemic Poisons Hepatotoxic Agents (Liver)
Carbon tetrachloride Tetrachloroethane
Neurotoxic Agents (Nerve System)
Methanol Carbon disulfide Metals (Pb, Hg) Organometallics Benzene
Nephrotoxic Agents (Kidneys)
Halogenated hydrocarbons
Hematopoietic Toxins (Blood)
Aniline Toluidine Nitrobenzene Benzene Phenols
Anesthetics/Narcotics (Consciousness)
Acetylene hydrocarbons Olefins
Ethyl ether, isopropyl ether Paraffinic hydrocarbons Aliphatic ketones Aliphatic alcohols Esters
Source:Clayton, G D., and F E Clayton, Patty’s Industrial Hygiene and Toxicology (New York: John Wiley and Sons, Inc., 1986).
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