Vaccari D.A., Strom P.F., Alleman J.E. Environmental Biology for Engineers and Scientists

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21.2.1 Toxic Effects

Tables 21.4 and 21.5 contains toxicity data on some pesticides. Most insecticides act by

interfering with the nervous system. For example, DDT binds to lipoproteins in axon

membrane, holding a gate open for sodium. Organochlorines in general stimulate the ner-

vous system, causing irritability, tremor, and convulsions.

OP and carbamate inhibit acetylcholinesterase. In the Central nervous system (CNS)

they cause tremor and convulsion. In the autonom ic nervous system they cause diarrhea,

involuntary urination, and bronchoconstriction. At the neuromuscular junction they cause

muscle contraction, weaknes s, and loss of reﬂexes, followed by paralysis. Chronic expo-

sure causes neuropathy (destruction of nerve ﬁbers). Motor effects predominate, includ-

ing muscle wasting, difﬁculty with movement, and inability to locate one’s joints in space,

making walking difﬁcult. Exposure to OPs were observed in both human and animal tests

to result in myopathy (damage to muscle tissue), including necrosis of skeletal muscles.

This is thoug ht to be caused by the high levels of acetylcholine resulting from inhibition

Dichlorodiphenyltrichloroethane (DDT)

Chlordane

Lindane (a fungicide)

Dieldrin

2,4-dichlorophenoxyacetic acid

(2,4-D)

HLORINATED INSECTICIDES

CCl Cl

CCl

CHLORINATED HERBICIDES

OCH

COOH

OCH

COOH

2,4,5-trichlorophenoxyacetic acid

(2,4,5-T)

Figure 21.1 Structures of some organochlorine pesticides.

808

TOX ICITY OF SPECIFIC SUBSTANCES

Parathion

Malathion

Carbar

l (Sevin) Atrazine (a triazine used as a herbicide)

Glyphosate − a herbicide

RGANOPHOSPHATE PESTICIDES

ONO

SCH

OHCCH

NCH

OH H

OOH

NITROGEN-BASED PESTICIDES

CARBAMATE INSECTICIDES

NHCH

NH CH

OCNHCH

Figure 21.2 Structures of some unchlorinated pesticides.

TABLE 21.4 Mammalian Toxicity of Some Insecticides

NOEL (mg/kg)

ADI

Pesticide (mg/kg) Rat Dog Human (mg/kg)

Diazinon 108 0.1 0.02 0.02 0.002

Dichlorvos 80 NA NA 0.033 0.004

Malathion 1375 5.0 0.2 NA 0.02

Parathion 13 NA NA 0.05 0.005

Trichlorfon 630 2.5 1.2 NA 0.005

Aldicarb 0.8 0.125 0.25 0.005

Carbaryl 850 10 NA 0.06 0.01

DDT 113 0.05 NA NA 0.01

Aldrin/dieldrin 40 0.025 0.025 NA 0.001

Chlordane 335 0.25 0.075 NA 0.001

Endrin 18 0.05 0.02 NA 0.0002

Heptachlor 100 0.25 0.0625 NA 0.0005

Lindane 88 1.25 1.6 NA 0.01

Methoxychlor 6000 10 NA NA 0.1

NA: Not available.

Source: Lu (1991).

PESTICIDES

809

of acetylcholinesterase. Symptoms include muscle tenderness. Adverse psychological dis-

turbances have been identiﬁed which lasted from six months to a year. These included

depression, nightmares, and emotional instability.

There is positive interaction between many OPs. One of the strongest is a 100-fold

increase in the combined toxici ty of malathion and tri-o-cresyl phosphate (TOCP).

Some pesticide formulations include potentiators to increase their effect, although this

TABLE 21.5 Acute Aquatic Toxicity of Example Pesticides

Photosyn. % Daphnia

Pesticide Red.

48-h EC

Amphipod Stoneﬂy Naiad Fish Tadpole

Organochlorine

Aldrin 85 28 9800 1.3 NA 150

Chlordane 94 29 26 15 69 NA

DDT 77 0.36 1.0 7.0 34 800–1000

Dieldrin 85 250 460 0.5 16 100–150

Endrin 46 20 3.0 0.25 1.3 120–180

Heptachlor 94 42 29 1.1 56 440

Lindane 28 460 48 4.5 56 2700–4400

Methoxychlor 81 0.78 0.8 1.4 35 330

Toxaphene 42 15 26 2.3 5.1 140–500

Organophosphorus

Diazinon 7 0.9 200 25 NA NA

Dibrom 56 0.35 110 8.0 NA 1700

Dichlorvos NA 0.066 0.5 0.1 NA NA

Malathion 7 1.8 1.8 10 12,500 200–420

Methyl parathion NA 0.14 NA NA 7,500 NA

Parathion NA 0.6 0.6 5.4 1,600 1000

Phosdrin NA 0.16 0.16 5.0 NA NA

Herbicides

Dinitrocresol NA 0.014

NA 0.32 NA NA

Diquat NA NA NA NA 91

2,4-D acid NA 1.4 NA 15 NA NA

2,4-D butoxyethanol NA >100

0.44 1.6 2.1

ester

Naphtha NA 3.7 0.84 2.8 NA NA

Paraquat NA 3.7 11 >100 400

Picloram NA NA 27 48 26.5

Silvex NA 2 NA 0.34 83

Triﬂuralin NA 0.24 2.2 3.0 8.4

0.1

2,4,5-T NA NA NA NA 0.5

The ﬁsh are freshwater fathead minnow for OC and OP pesticides, and bluegill for the herbicides; 96-h LC50

except where noted. Concentrations in mg/L for organochlorine and organophosphorus pesticides and mg/L

for herbicides. NA, not available.

Reduction of estuarine phytoplankton photosynthetic productivity during 4 h exposed to a concentration

of 1.0 mg/L.

26-h EC

48-h LC

24-h LC

Source: Connell and Miller (1984).

810 TOXICITY OF SPECIFIC SUBSTANCES

increases mammalian toxicity. Antagonistic effects occur as well. Substituted urea herbi-

cides reduce the toxicity of parathion, probably by inducing MFO detoxiﬁcation.

OP and carbamates are not carcinogens, in general, except some that are chlorinated, or

some like carbaryl, which can be nitrosated to a carcinogenic form. All organochlorines

cause hepatoma in mice. DDT is controversial because it does not cause cancer in rats,

hamsters, and a few other animals. Only for hexachlorocyclohexane is there epidemiolo-

gical evidence of cancer in humans. The fumigants ethylene dibromide (EDB) and 1,2-

dibromo-3-chloropropane (DBCP) cause stomach cancer in rats and mice and have been

restricted. The herbicide amitrole (aminotriazole) and the ethylenebisdithiocarbamates

(such as maneb) produce thyroid tumors. Carbaryl (sevin) is a teratogen in dogs but

not in other animals. The dithiocarbamate fungicides, captan, paraquat, and others, are

reportedly teratogenic. The herbicide 2,4,5-T is known to cause teratological effects in

rats.

Carbaryl produced effects attributed to decr eased renal resorption in human experi-

ments. Paraquat causes edema, hemorrhage, and ﬁbrosis in the lungs when inhaled. Pyr-

ethrum is associated with hypersensitivity, contact dermatitis, and asthma. OCs are

hepatotoxic and induce microsomal monooxygenases. Some pesticides from all the

major groups have an effect on the immune system. These include malathion, methylpar-

athion, carbaryl, DDT, paraquat, and diquat.

Herbicides act on plants by affecting either growth or photosynthesis. The phenoxya-

cids simulate natural auxins (plant growth hormones). Urea herbicides inhibit photosys-

tem II, preventing ATP and NADPH formation. Diquat and paraquat inhibit photosynthesis.

Some are selective for either monocots (grassy plants) or dicots (broadleaf).

The manufacture of the pesticide 2,4,5-T produces 2,3,7,8-tetrachlorodibenzo-

p-dioxin (TCDD) as a trace impurity. This is one of the most toxic substances known.

The manufacture and use of 2,4,5-T and related herbicides has resulted in some of the

most notorious environmental contamination incidents known, which involve TCDD

(see Section 21.4).

Dinitrophenols are used for weed control. They uncouple oxidative phosphorylation in

respiration, causing metabolic activity to increase out of control. Effects of acute exposure

in humans include the sensation of heat, and rapid breathing and heart rate. Chronic symp-

toms include anxiety, sweating, thirst, and fatigue. Paraquat causes lung, kidney, and liver

damage and can cause pulmonary ﬁbrosis even from routes other than inhalation.

Fate and Transport: Dieldrin depuration half-life ranges from 148 days for the guppy

Lebistes reticulatus to 12.2 days for tubiﬁcid worms (Tubifex sp.). Depuration half-lives

are correlated with lipophilicity. Plants cannot excrete toxins, but instead, segregate them

in vacuoles within the cells. Table 21.6 summarizes some of the environmental fate and

transport properties for a number of pesticides.

21.2.2 Ecosystem Effects

Biomagniﬁcation is a problem mostly with organochlorine pesticides. The classic case is

DDT and its metabolite DDD. Figure 18.9 illustrates two examples of organochlorine bio-

magniﬁcation.

By their very nature, pesticides can produce pronounced effects on populations and

ecosystems. These include many that were dramatically publicized by Rachel Carson

in her book Silent Spring, including ﬁsh and bird kills, development of insect resistance,

and actually causing an increase in some pests by destroying their predators. In the latter

PESTICIDES 811

case, the target species is sometimes the beneﬁciary of a pesticide application, if its pre-

dators and competitors are more strongly affected. An example of this counterproductive

situation is the application of pesticide to control boll weevils and leafworms infesting

cotton farms in Central America. From 1950 to 1955 the number of pesticide applications

had to increase from few or none to 8 to 10 per season. By 1960, 28 applications per sea-

son were needed. Over the same period, the number of pest species increased from the

original two in 1950, to ﬁve in 1955, and then eight in 1960. Many similar examples exist.

Many pesticides, such as insecticides, fungicides, and fumigants, target soil organisms

and have their greatest environmental effect on nontarget organisms in the soil. Suscep-

tible invertebrates include insects, earthworms, slugs, and gastropods. Some of these

organisms contribute to topsoil formation. Insecticides applied to natural systems, such

as for the control of forest pests, can reduce the species diversity within the invertebrates.

Among the terrestrial vertebrates, avian species are especially susceptible to the insec-

ticides. LD

values are often less than 100 mg/kg. However, the subleth al effects are of

greatest concern. In particular, bird reproduction is very sensitive to organochlorine insec-

ticides. The best known effect is the thinning of eggshells due to DDT, its metabolite

DDE, and dieldrin, among others. Th ese prevent the embryos from surviving to hatch.

However, many other reproductive effects are also found, including direct embryo toxicity

TABLE 21.6 Fate and Transport Properties of Some Pesticides

Aqueous Log

BCF Typical

Pesticide Solubility (mg/L) Log

(Fish) (L/kg) Environmental Half-Life

Organochlorines 1–12 years

2,3,7,8-TCDD 0.0002 6.15 4.73

DDT 0.0012 5.98 4.78

Aldrin 0.01

Chlordane 0.056 5.15 4.05 >100 days

Heptachlor 0.056

Dieldrin 0.18 5.48 3.76

Lindane 7.0 4.82 2.51 >100 days

Organophosphates 72–180 days

Chlorpyrophos 0.3 4.99 2.65

Parathion 24

Diazinon 40

Malathion 145 <30 days

Dimethoate 2,500

Carbamates 20–365 days

Carbaryl 40

Carbofuran 700

Pyrethrin <1day

Herbicides

Simazine 5.0 30–100 days

Atrazine 34 30–100 days

2,4,5-T 280 0.6 1.63 <30 days

2,4-D 890 1.57 1.30 <30 days

Glyphosate 12,000 30–100 days

Diquat (70%)

Dalapon (80%)

Source: Rand and Petrucelli (1985); LaGrega et al. (2001); Rao et al. (2004); Ferruzzi and Gan (2004).

812 TOXICITY OF SPECIFIC SUBSTANCES

and aberrant parental behavior such as destruction of eggs. The greatest concern with

these effects is with birds of prey, because the organochlorine pesticides are biomagniﬁed.

Species that have experienced serious population declines include the bald eagle (Halia-

cetus leucophalus) and the osprey (Pondion haliatetus).

DDT has not been found to seriously affect wild mammals. However, other organo-

chlorine pesticides, especially the cyclodienes such as heptachlor, dieldrin, and endrin ,

have resulted in mortalities. Although the cholinesterase inhibitors are very toxic to

mammals, no signiﬁcant effects have been observed in the wild. Development of resis-

tance has been observed in a variety of aquatic invertebrates.

Aquatic ecosystems have been affected both by direct application of pesticides, such as

for control of mosquitoes, and by runoff from agricultural, forest spraying, and so on.

Arthropods such as crustraceans are very susceptible to insecticides. Heavy killings of

crabs and shrimp have occurred in marshes sprayed with organochlorines. The microcrus-

taceans are an important component of the food chain and are also affected heavily.

Mollusks and annelids, on the other hand, are relatively tolerant. Fish tend to be very sus-

ceptible to the organochlorines, especially the cyclodienes. Some warm-water, rapidly

reproducing speci es of ﬁsh in heavily sprayed areas of Mississippi have become resistant

to levels of some of the organochlorines 100 times higher than that which is normally

toxic.

Chronic toxicity is repor ted as the MATC in Section 19.7. Application factors (LC

MATC) for chronic toxicity vary greatly. For Kepone the application factor for sheeps-

head minnows ranges from 0.001 to 0.002. However, for endrin the AP is 0.35 to 0.91.

In other words, Kepone causes chronic effects at concentrations as much as 1000 times

lower than the LC

, whereas the chron ic effects of endrin do not appear until the con-

centration reaches one-third of the LC

Pesticides interact with each other, often positively. The toxicity of pesticides to aqua-

tic organisms als o interacts with the abiotic factors temperature and pH, as described in

Section 17.3. Both positive and negative effects of temperature have been observed. End-

rin was found to be several hundred times as toxic to carp ( Cyprinus carpio )at27



Casit

was at 7



C. DDT and methoxychlor, on the other hand, were more toxic at lower tempera-

tures. Hardness does not seem to produce an effect independent of pH, and many of the

pH effects are associated with ionizable pesticides or those that react to form other pro-

ducts at certain pH ranges.

21.3 HYDROCARBONS, SOLVENTS, PAHs, AND SIMILAR

COMPOUNDS

Here we consider other anthropogenic organic chemicals and their by-products. Solvents

include many types of liquid hydrocarbons, which are used as carriers for other materials,

such as pigments in paints, or for rinsing oil and grease from manufactured items. Some,

such as benzene, may also be components of fuel or raw materials for synthesis of other

compounds. Some of the larger molecules we consider include the polynuclear aromatic

hydrocarbons (PAHs), phthalate esters, and surfactants. Chlorinated organics are consid-

ered separately in the next section.

Many hydrocarbons are biotransformed by cytochrome P450 enzymes. Thus, they can

interact with other toxins either positively by increasing cytochrome activity (as benzene

does) or negatively by competing for the enzyme (as toluene does with benzene).

HYDROCARBONS, SOLVENTS, PAHs, AND SIMILAR COMPOUN DS 813

The solvents are hydrocarbons up to ﬁve or six carbons in size. They have appreciable

vapor pressures, which may result in signiﬁcant inhalation exposure. Solvents are also

absorbed signiﬁcantly through the skin in occupational settings. The larger compounds

are more likely to be adsorbed to particles. Exposure can result from inhalati on or inges-

tion of the particles. Some of them enter the food chain, where they can be bioaccumu-

lated and ingested.

The major toxic effects common to these compounds are CNS depression, including

narcosis, and irritati on. These are of special concern with acute exposure to the solvents.

However, these types of compounds can cause other effects, ranging from liver or kidney

damage to carcinogenesis. CNS depression is essentially the action of a general anaes-

thetic. The potency of organics to produce CNS depression increases with the chain length

of the compound. Halogenation, addition of an alcohol group, or unsaturation (removal of

hydrogen to form a double carbon–carbon bond) increase potency as well.

One mechanism of irritation by hydrocarbons and surfactants is by the extraction of

fats from the skin, lungs, eyes, or other cell membranes contacted. Addition of functional

groups to an organic molecule tends to increase irritant properties. Amines and acidic

groups make the compound corrosive, and alcohol, aldehyde, and ketone groups can pre-

cipitate and denature proteins associated with the membr anes.

The aliphatic (saturated) hydrocarbons have relatively less toxicity than others do in

this group. Ingestion of more than 1 mL/kg can produce systemic effects. For lower

amounts, aspiration to the lungs is the principal concern. Chronic exposure, such as to

hexane or heptane, produces neuropathy, probably due to metabolism to alcoholic and

ketone forms. Oleﬁnic (unsaturated) forms are stronger CNS depressants. Interestingly,

the presence of doubl e bonds eliminates the neurotoxicity of hexane and heptane. The

cyclic hydrocarbons, such as cyclohexane, are similar to the open-chain forms, except

that they are higher in irritancy, and do not seem to produce chronic effects.

Alcohols, including glycols, are much stronger CNS depressants than aliphatics are and

slightly mor e irritating. As carbon chain length increases, irritation decreases but lipophi-

licity increases, as does systemic toxicity. Methanol is less inebriating than ethanol but

has the unusual property of destroying the optic nerve. Fifteen milliliters can cause blind-

ness. As with ethanol, it is metabolized by a zero-order rate mechanism, but at one-

seventh the rate. Ethanol acts as an irritant by dehydrating protoplasm. An initial stimu-

lant effect is caused by depression of control mechanisms in the brain. Pain sensitivity is

greatly reduced. Cutaneous (skin) blood vessels become dilated. The resulting increased

heat loss can be dangerous in cold weather. It increases gastric secretion, which can aggra-

vate stomach ulcers. It causes fat accumulation and cirrhosis in the liver. The latter can be

fatal itself or can cause progression to cancer. Ethanol increases urine ﬂow through a

mechanism involving pituitary and adrenal hormones. The resulting water loss, along

with the acetaldehyde by-product, may be a cause of the headache in a hangover. On

the other hand, there is evidence that consumption of small amou nts of alcoholic bev-

erages with meals may have some beneﬁts for the cardiovascular system.

Isopropyl alcohol is less toxic than n-propanol, but both these and butanol are more

toxic than ethanol. Allyl alcohol is highly irritating. It can be absorbed through the

skin, resulting in deep pain and possible burns of the eye. Glycols are compounds that

have two hydroxyls on adjacent carbons. They are less toxic than the monohydroxy alco-

hols. Ethylene glycol can be fatal to humans with a single dose of 100 mL. It is biotrans-

formed to oxalic acid, which blocks kidney function. Ethanol can inhibit this

transformation, making it an antidote.

814 TOXICITY OF SPECIFIC SUBSTANCES

Aldehydes tend to be more irritating than they are CNS depressants. One unique toxi-

city of the aldehydes, especially formaldehyde, is sensitization. That is, it can increase a

person’s response to other chemicals. Formaldehyde is a common industrial chemical

used in plastics and resins. The LD

in humans for formalin (37 to 50% formaldehyde

solution) is about 45 g, although deaths have been reported at as low as 30 g. Ingestion can

produce headaches, GI tract corrosion, pulmonary edema, fatty liver, kidney necrosis,

unconsciousness, and vascular collapse. Formaldehyde has been associated with muta-

genicity and carcinogenicity in laboratory tests, but a steep dose–response relationship,

the lack of epidemiological evidence for carc inogenicity in humans, plus the following

facts, suggest the presence of a carcinogenicity threshold. Formaldehyde is a metabolic

by-product, normally present at several ppm in tissues. Thus, it appears that carcinogeni-

city is associated with exposures high enough to cause irritation and tissue injury. Acet-

aldehyde is less irritating and toxic. Acrolein is an unsaturated propionaldehyde. The

double bond greatly increases its reactivity as well as its irritant and toxic effect.

Ketones produce fewer occupational health problems, possibly because their irritant

properties serve as a warning before other effects occur. Acetone causes skin irritation

only after repeated lengthy contact. Eye irritation occurs with unacclimated persons at

air concentrations of 500 ppmv, and repeated exposure can produce tolerance up to

2500 ppmv. Carboxylic acids are mostly irritants. Acidity, and irritation, decreases with

chain length and increases with halogenation. Esters are stronger anesthetics than alco-

hols. The lower-carbon esters are stronger irritants than alcohols and can cause lacrima-

tion (eye tearing). Phosphate esters are used as plasticizers and can cause CNS damage.

Ethers are effective anesthetics and slightly irritat ing.

Amines have many uses, including as disinfectants in consumer products. They include

some of the most toxic common industrial chemicals. Most simple amines have pK

values between 10.5 and 11.0, making them ionized at physiological pH and corrosive

to tissues.

primary

amine

secondary

amine

tertiary

amine

An important property of amines is that they are easily absorbed by all routes of expo-

sure, including the skin. Thus, the dermal toxicity is often similar to the ingested toxicity

(Table 21.7). Systemic effects include pulmonary edema and hemorrhage, liver and

TABLE 21.7 Toxicity of Some Amines in Animal Tests (mg/kg)

Amine Oral LD

Skin LD

Methylamine 0.02 0.04

Ethylamine 0.4 0.4

Propylamine 0.4 0.4

Butylamine 0.5 0.5

Hexylamine 0.7 0.5

Source: Williams and Burson (1985).

HYDROCARBONS, SOLVENTS, PAHs, AND SIMILAR COMPOUN DS

815

kidney necrosis, and coronary degeneration. They react to form methemoglobin in the

blood. Repeated exposure can produce strong allergic reactions. Aromatic amines or

diphenylamine comp ounds are carcinogens, such as benzidine, 2-naphthylamine, or 4-

aminodiphenyl, which cause ‘‘aniline tumors’’ in dye industry workers. Any alkyl

amine (such as those that can be produced in digestion of food) can react with nitrites

in food and acid in the stomach to form nitrosamines, which can potentially cause liver

cancer.

Analine itself is an important industrial compound that is also used in household pro-

ducts such as polishes, paints, and inks. It is considered very toxic and is easily absorbed

through the skin. In the blood, aniline oxidize s Fe(II) to Fe(III), turning the blood to a

brown-black color and eliminating its ability to transport oxy gen.

Nitro compounds are mild irritants. Unsaturated compounds are easily absorbed der-

mally. Nitrated aromatics produce a variety of effects, including methemoglobinemia.

Some produce bladder tumors. Trinitrotoluene and dinitrobenzene are easily absorbed

by all routes of exposure. Besides the other toxic effects, they can uncouple oxidative

phosphorylation and cause liver damage. Nitriles (compounds with structure RC



are easily absorbed, and many slowly degrade to cyanide. Acetonitrile is considered

moderately to very toxic. Acrylonitrile is classiﬁed as highly toxic and is a suspected

human carcinogen.



CHC



acrylonitrile

Single-ring aromatics include benzene and its derivatives. Aromatics tend to be more

toxic than aliphatics with a similar number of carbons. CNS depression caused by aro-

matics differs qualitatively from that produced by aliphatics. Coma induced by aliphatics,

such as by gasoline, exhibit inhibited reﬂexes. On the other hand, aromatics produce

hyperactive reﬂexes, sometimes with convulsions.

Benzene is reportedly fatal at about 10 to 15 mL for an adult, and possibly as low as 2

to 5 mL. Inhalation at 250 ppmv produces headache, nausea, vertigo, and drowsiness;

3000 ppmv in air is irritating to the eyes and respirato ry tract. Acute symptoms appear

after 30 to 60 minutes at 7500 ppmv; 20,000 ppmv for 5 to 10 minutes has been reported

to be fatal. Acute symptoms are respiratory inﬂammation, pulmonary edema and hemor-

rhage, renal congestion, and cerebral edema. Chronic dermal exposure can produce

damage resembling ﬁrst- or secon d-degree burns. Blood disorders progress through

three stages: First is a reversible reduction in blood clotting and a mild anemia. Continued

exposure produces increased leukocyte production. Finally, a more severe anemia and

hemorrhage occurs. Less com monly, benzene also causes a cancer, leukemia. It is a

class A carcinogen. Chomosome damage has also been observed in humans. Toluene is

a stronger CNS depressant than benzene but is not known to cause permanent blood dis-

orders. The xylenes are even strong er CNS depressants than toluene.

Phenols are cytotoxic, acting as a local anesthetic and CNS depressant. They are easily

absorbed but produce strong irritation and burns. Phenol easily penetrates the skin, where

it causes deep burns. Burns from ingestion can lead to extreme shock and death. Phenol

can also cause necrosis systemically in the liver and kidneys as well as the heart and urin-

ary tract. Death from systemic poisoning is usually from respiratory depression as a result

of its CNS depression activity. Ingestion of as little as 1 or 2 g reportedly can be fatal. The

816 TOXICITY OF SPECIFIC SUBSTANCES

dihydroxyphenols catechol, resorcinol and hydroquinone, and cresol, behave similarly to

phenol, except that they are more toxic.

benzene

phenol

hydroquinone

p-cresol

Polynuclear aromatic hydrocarbons (PAHs, also referred to as PNAs or polycyclic aro-

matic hydrocarbons) are fused benzene rings and their derivatives. Many are prevalent in

coal and crude oil. They also are signiﬁcant produc ts of partial combustion; that is, they

are found in soot and smoke particles, and in pyrolytically produced tars and oils. The

simplest PAH is naphthalene.

naphthalene

anthracene phenanthrene

pyrene

benzo[a]pyrene

fluorenefluoranthene

PAHs are strongly absorbed to soil and sediment particles in the environment and can

even be transported long d istanc es by the wind. Aqueous solubility decreases with molar

mass and is lower for linear ring arrangements than more condensed forms (compare

anthracene and phenanthrene in Table 21.8). In aquatic environments, PAHs tend to

be most concentrated in sediments, least in the water column, and intermediate in organisms.

Some bacteria and fungi can mineralize some PAHs, but others can only cometabolize

them. Fungi and some animals utilize the cytochrome P450 (MFO) system to hydroxylate

PAHs to diols. Certain intermediates of this conversion in mammals are thought to be

responsible for carcinogenicity in this group. Injection of PAHs in ﬁsh can induce

MFO activity severalfold within several days.

PAHs cause acute toxic effects in humans only at high doses that are not common

in environmental or occupational settings. Napthalene inhalation cause s headache,

confusion, nausea, and profuse perspiration in humans. For a variety of marine and

HYDROCARBONS, SOLVENTS, PAHs, AND SIMILAR COMPOUN DS 817