Only after the last tree has been cut down.  Only after the last river has been poisoned.  Only after the last fish has been caught.  Only then will you find that money cannot be eaten.

"When an activity raises threats of harm to human health or the environment, precautionary measures should be taken even if some cause and effect relationships are not fully established scientifically. In this context the proponent of an activity, rather than the public, should bear the burden of proof." - Wingspread Statement of the Precautionary Principle.

Potential Health Effects of Odor From Animal Operations, Wastewater Treatment, and Recycling of Byproducts

Susan S. Schiffman, PhD, Duke University, NC
John M. Walker, PhD, US EPA, Office of Water (sludge office)
Pam Dalton, PhD
Tyler S. Lorig, PhD
James H. Raymer, PhD
Dennis Shusterman, MD
C. Mike Williams, PhD

ABSTRACT. Complaints of health symptoms from ambient odors have become more frequent in communities with confined animal facilities, wastewater treatment plants, AND BIOSOLIDS RECYCLING OPERATIONS.

The most frequently reported health complaints include eye, nose, and throat irritation, headache, nausea, diarrhea, hoarseness, sore throat, cough, chest tightness, nasal congestion, palpitations, shortness of breath, stress, drowsiness, and alterations in mood.

Typically, these symptoms occur at the time of exposure and remit after a short period of time. However, for sensitive individuals such as asthmatic patients, exposure to odors may induce health symptoms that persist for longer periods of time as well as aggravate existing medical conditions.

A workshop was held at Duke University on April 16-17, 1998 cosponsored by Duke University, the Environmental Protection Agency (EPA), and National Institute on Deafness and Other Communication Disorders (NIDCD) to assess the current state of knowledge regarding the health effects of ambient odors.

This report summarizes the conclusions from the Workshop regarding the potential mechanisms responsible for health symptoms from ambient odors. Methods for validation of health symptoms, presence of odor, and efficacy of odor management techniques are described as well.

(Article copies available for a fee from The Haworth Document Delivery Service: 1-800-342-9678. E-mail address: Website:



KEYWORDS:   Health effects, odor, nasal irritation, irritant, confined animal feeding operations (CAFOs), dust, particulates, wastewater treatment, BIOSOLIDS, composting.

Special emphasis was placed on potential health issues related to odorous emissions from animal manures AND OTHER BIOSOLIDS.

Odors are sensations that occur when a complex mixture of compounds (called odorants) stimulate receptors in the nasal cavity. Most odorants associated with animalsí manures AND BIOSOLIDS are volatile organic compounds (VOC's) that are generated by bacterial degradation of protein, fat, and carbohydrates in the organic matter. Reactive inorganic gases such as AMMONIA and hydrogen sulfide are also important odorants that can be emitted from animal manures AND BIOSOLIDS.


Workshop participants discussed three paradigms by which ambient odors may produce health symptoms in communities with odorous manures AND BIOSOLIDS.

In the first paradigm, the symptoms are induced by exposure to odorants at levels that also cause irritation (or other toxicological effects). That is, irritation -- rather than the odor -- is the cause of the symptoms, and odor simply serves as an exposure marker.

In this paradigm irritancy (or other toxicity) generally occurs at a concentration somewhat higher (about 3 to 10 times higher) than the concentration at which odor is first detected (odor threshold).

While the concentration of each individual compound identified in odorous air from agricultural and municipal wastewater facilities seldom exceeds the concentration that is known to cause irritation, the combined load of the mixture of odorants can exceed the irritation threshold. That is, the irritation induced by the mixture derives from the addition (and sometimes synergism) of individual component VOCs.

In the second paradigm health symptoms occur at odorant concentrations that are not irritating. This typically occurs with exposure to certain odorant classes such as sulfur-containing compounds and organic amines at concentrations that are above odor detection thresholds but far below irritant thresholds.


Health symptoms often reported include a stinging sensation, nausea, vomiting, and headaches. The mechanism by which health symptoms are induced by sulfur gases or organic amines for which odorant potency far exceeds the irritant potency is not well understood.

Noxious odors that are neither irritating nor toxic can set up a cascade of events such as physiological stress or nutritional problems (caused by altered food intake) that lead to health effects. The genetic basis of aversions to malodors is not well understood, but brain imaging studies suggest that noxious odors stimulate different brain areas than those that process pleasant odors.

In the third paradigm, the odorant is part of a mixture that contains a co-pollutant that is essentially responsible for the reported health symptom. Odorous airborne emissions from confined animal housing, composting facilities, AND LAND APPLICATION OF SLUDGE can contain other components that may be the cause of the symptoms such as bioaerosols consisting of endotoxin, dust from food, airborne manure particulates, glucans, allergens, microorganisms, or toxins.

Thus, an individual may encounter odors from swine facilities while simultaneously exposed to dust or gram-negative endotoxin. In this case, the symptoms or health effects are more likely to result from the irritant effects of the dust or from other inflammatory responses to endotoxin exposure rather than from odor.


A majority of the studies reviewed in this report are taken from laboratory experiments where greater control is possible and mostly not from confined animal feeding operations, municipal wastewater or BIOSOLIDS treatment, OR THE RECYCLING of these byproducts.


By the review of these studies, examples are given that can help elucidate the types of health symptoms that may occur from exposure to odorous volatile compounds and associated particulates from animal feeding and the processing and recycling of animal manures AND BIOSOLIDS.

In addition, this review helps establish a basis for future management and research regarding the potential impacts of odor on human health from such operations.

The odor exposures that have received the greatest research attention are those that involve irritation. Physiological responses to irritation in the upper respiratory trace (nose, larynx) and/or lower respiratory tract (trachea, bronchi, deep lung sites) have been documented in both humans and animals.

Irritation of the respiratory tract can alter respiratory rate, reduce respiratory volume (the amount of air inhaled), increase duration of expiration, alter spontaneous body movements, contract the larynx and bronchi, increase epinephrine secretion, increase nasal secretions, increase nasal airflow resistance, slow the heart rate, constrict peripheral blood vessels, increase blood pressure, decrease blood flow to the lungs, and cause sneezing, tearing, and hoarseness.

Release of the potent hormone epinephrine (also called adrenalin) subsequent to nasal irritation may be a source of feelings of anger and tension that have been reported by persons exposed to odors. Epidemiological studies in communities with animal operations and municipal wastewater facilities have reported increased occurrence of self-reported health symptoms consistent with exposure to irritants.

The odorous emissions that reach neighbors of animal and municipal wastewater facilities AND RECYCLING OPERATIONS are a function of the concentration of volatiles produced at the source as well as their emission rates, dispersion, deposition, and degradation in the downwind plume.

Furthermore, numerous sources at a facility can contribute to the total odor and irritation intensity experienced by neighbors.

Workshop participants concluded that current evidence suggests that the symptom complaints experienced by neighbors of some odorous animal operations and municipal wastewater facilities may constitute health effects.


This report summarizes (the) current state of knowledge regarding the health effects of ambient odors with special emphasis on odorous emissions from animal manures AND OTHER BIOSOLIDS. The potential mechanisms that are responsible for health symptoms are discussed.


The most common health complaints associated with environmental odors from agricultural sources AND BIOSOLIDS include eye, nose, and throat irritation, headache, nausea, hoarseness, cough, nasal congestion, palpitations, shortness of breath, "stress", drowsiness, and alterations in mood.

These symptoms attributed to odors are generally acute in onset (occur at the time of exposure) and self-limited in duration (remit after a short period of time).

Persons with allergies and asthma often assert that odors exacerbate their symptoms. Persons who report adverse health symptoms from odors usually indicate that they have problems with numerous types of odorous compounds.



Health symptoms from odors can potentially result from two sources: the odor (the sensation) or the odorant (the chemical or mixture of chemicals that happens to have an odor).

Odor sensations are induced when odorants interact with receptors in the olfactory epithelium in the top of the nasal cavity. Signals from activated receptors are transmitted via the olfactory nerve (first cranial nerve) to the olfactory bulb and ultimately to the brain.

Some reactive inorganic gases such as AMMONIA and H2S can also be odorants.

Odorants can also stimulate free nerve endings of four other cranial nerves (trigeminal, vagus, chorda tympani, and glossopharyngeal nerves) to induce sensations of irritation.

Sensory neurons of the trigeminal nerve innervate the eyes, nose, anterior 2/3 of the tongue, gums, and cheeks. The trigeminal nerve responds to five different classes of stimuli: (1) chemical, (2) mechanical (such as dust particles that touch the mucous linings of the nose, eye, or mouth), (3) thermal (temperature), (4) nociceptive (pain), and (5) proprioceptive (movement/position).

Trigeminal stimulation by odorous chemicals and dust induces sensations such as irritation, tickling, burning, stinging, scratching, prickling, and itching.

Free nerve endings of the vagus nerve transmit information on irritation in the throat, trachea, and lungs. Free nerve endings of the chorda tympani nerve (along with the trigeminal nerve) medicate irritation on the anterior tongue during mouth breathing; free nerve endings of the glossopharyngeal nerve transmit information about irritation on the posterior tongue.


Overall, the same compound can generate sensations of both odor and irritation, but the concentration necessary to elicit irritation is generally higher than that needed for odor.

Almost any airborne chemical can, in sufficient concentration, stimulate chemosensory trigeminal receptors in the nose and eyes, damage tissue, or cause toxic effects.


There are at least three paradigms that may explain how odors or odorants could potentially affect human health. In Paradigm l, the symptoms are induced by exposure to an odorant at levels that also cause irritation (or other toxicological effects).

In this case, irritation -- rather than the odor -- is the cause of the symptoms, and odor simply serves as an exposure marker. For odorants acting under Paradigm l, the irritancy (or other toxicity) generally occurs at a concentration above -- but within an order of magnitude -- of the odor threshold.

That is, the detection threshold for irritancy (concentration at which irritancy is first detected) is between 3 - 10 times higher than the concentration at which odor is first detected. (The odor detection threshold is the concentration at which odor is first detected.) Examples include AMMONIA, chlorine, and formaldehyde ......

At concentrations above the irritant threshold, both odor and irritant sensations can coexist. The sensation of odor is merely coincident with the more relevant irritative process; symptoms are more likely caused by irritation rather than "odor-induced." In this paradigm, odor is a warning of potential health symptoms at elevated concentrations.

In Paradigm 2, by contrast, exposure to odorous compounds at concentrations above the odor threshold but below irritant levels is associated with health symptoms.

This typically occurs with exposure to certain odorant classes such as sulfur-containing compounds and organic amines with odor thresholds that are 3 - 4 orders of magnitude (that is 10/3 and 10/4 times) below the levels that cause classical toxicological or irritant symptoms.

Industrial and biological sulfur gases (e.g. hydrogen sulfide, mercaptans, or thiophenes) have odor thresholds in the ppb (parts per billion) or ppt (parts per trillion range but they do not produce objective mucous membrane irritation until they reach a level of 10 - 20 ppm (parts per million.)

Nevertheless, health symptoms are often reported from residents of communities exposed to industrial sulfur gases and other malodorous compounds at levels exceeding the odor threshold but below irritant thresholds.


The third paradigm in which odors may be associated with symptoms is one in which the odorant is part of a mixture that contains a co-pollutant that is actually responsible for the reported health symptom. Odorous airborne emissions from confined animal operations, composting facilities, AND SLUDGE can contain other components that may be the cause of the symptoms such as bioaerosols consisting of endotoxin, dust from food, airborne manure particulates, glucans, allergens, microorganisms, or toxics.

It should be noted that odor perception is not always an adequate warning of impending toxicity. This situation arises when a compound is toxic or irritating at concentrations below the odor threshold. --------

A few compounds produce irritation almost in the absence of odor; for example, CO2 is an irritant that produces minimal, if any, odor response in humans.


There is experimental evidence to support each of the paradigms given above. This evidence is described below in order to elucidate the mechanisms by which odorous emissions can cause health symptoms.



There is extensive evidence that odorous volatile compounds can produce irritation in both the upper respiratory tract (nose, larynx) and lower respiratory tract (trachea, bronchi, deep lung sites).

This irritation involves both sensory signals (mediated by the trigeminal and vagus nerves) as well as actual inflammation of tissues.

Sensory irritation can arise: (1) from a single odorous compound above its irritant threshold, (2) from the aggregate effect of low concentrations of odorous chemicals not normally considered to be irritants, or (3) from weak trigeminal stimulation in combination with much higher levels of olfactory stimulation.

The fact that mixtures of low concentrations of odorants can induce sensory irritation is due to the fact that the primary mixture constituents can be additive (or, in some cases, even synergistic) in their ability to produce irritation, i.e. the irritancy of the mixture may, in some cases, be greater than the sum of the individual components. Even subthreshold levels of individual volatile organic compounds (VOCs) can add together when delivered in a mixture to produce noticeable sensory irritation.


However, the mixture of volatile compounds emitted from manures AND BIOSOLIDS does have the potential to cause sensory irritation with or without health complaints.


Administration of irritant compounds to the upper and/or lower airway in laboratory studies produces many systemic responses including: (1) changes in respiratory rate, depending upon the primary level of irritation (upper versus lower), (2) reduced respiratory volume, (3) increased duration of expiration, (4) alterations in spontaneous body movements, (5) contraction of the larynx and bronchi, (6) increased epinephrine secretion, (7) increased nasal secretion, (8) increased nasal airflow resistance, (9) increased bronchial tone, (10) decreased pulmonary ventilation, (11) bradycardia, (12) peripheral vasoconstriction, (13) increased blood pressure, (14) closure of the glottis, (15) sneezing, (16) closure of the nares, (17) decreased pulmonary blood flow, (18) decreased renal blood flow and clearance, and (19) lacrimation or tearing.

Irritants can also induce hoarseness of voice and impair mucociliary clearance functioning.

These physiological responses suggest that the respiratory system may be at risk from harmful substances. Reflexive breath stoppage (apnea) subsequent to stimulation of the trigeminal nerve in the upper airway is probably a defensive device to prevent inhaling chemicals in the air that might damage the lungs or respiratory tract.

This breath stoppage does not occur in isolation as evidenced by a subsequent cascade of physiological symptoms associated with this response. This nasal reflex induces activity in the sympathetic division of the autonomic nervous system (ANS) leading to increasing in circulating epinephrine.

This causes acceleration of heart rate and peripheral vasoconstriction (leading to an increase in blood pressure). In addition, activity in the sympathetic division of the ANS is often associated with emotional induction of fear or anger.

Sustained exposure to irritating solvents can also impact neurobehavioral functioning.


These factors, along with the unpleasant sensory properties of irritation, make strong trigeminal stimulation a memorable event, one which is likely to be regarded as highly aversive.

Lower airway irritation usually produces an increase in breathing rate and pulmonary ventilation and little change in heart rate or blood pressure. There are instances, however, in which lower airway irritation can cause decreased respiratory rate (postexpiratory apnea).

Volatile chemical irritants can also cause local redness, edema, pruritis or pain, and eventually altered function. Excessive irritation in the lower airway (as well as upper airway) may lead to tissue damage and, eventually, scarring. Airway irritation is also associated with non-respiratory tract health complaints such as headache and lassitude.


Two types of nerve fibers in the trigeminal nerve conduct nociceptive (pain) afferent pules: finely myelinated A-delta fibers and un-myelinated C fibers.

Dull and burning painful sensations are characteristic of C fibers while sharp, stinging sensations appear after activation of A-delta fibers.

Activation of trigeminal C fibers by irritants leads to the release of neuropeptides including substance P into the nose. Substance P induces neurogenic inflammation including vasodilation, increased blood flow, increased vascular permeability, increased ocular pressure and pupillary contraction.

Substance P release is associated with an increased presence of polymorphonuclear neutrophilic leukocytes (PMNs) in the nasal cavity which indicates the presence of acute inflammation.

Exposure to 25 mg/m3 VOCs for 4 hours led to increased levels of PMNs in nasal lavage fluid. The release of substance P by trigeminal stimuli is also one potential mechanism by which trigeminal irritants may cause head pain.

Vasculature in the cranium is supplied by substance P-containing C fibers of the trigeminal nerve. Thus, inhaled irritants in the air may induce headaches and migraines by increasing cortical blood flow via the trigeminovascular system, i.e. via stimulation of a sensory (trigeminal) nerve.


There is often a temporal disparity between odor and irritant sensations with odor sensations tending to precede the irritant sensations. This is due in part to the fact that chemical agents must migrate through the mucosa to activate free nerve endings of the trigeminal nerve.

This fact coupled with the relatively slow transmission time of the C fibers leads to a slowly responding system in comparison to olfaction. Sensations of odor and irritation also respond different to continuous chemosensory stimulation. Odor sensations tend to fade quickly (adaptation) upon stimulation while irritancy can grow sharply over a period of time though it may ultimately adapt to some degree by six hours of exposure.

The growth of irritancy over time may be due in part to the kinetics of overcoming the buffering capacity of nasal mucus or may represent cumulative damage to structural elements.

Thus, odor is a warning of potential health symptoms from irritation at elevated concentrations. Continuous exposure to compounds such as AMMONIA or H2S can lead to odor fatigue and/or tolerance, and this reduced sensitivity may jeopardize health when the warning signal is not adequately perceived.


Odorous VOCs have been found in the blood and brain after three hours of exposure, and olfactory receptors have been shown to respond to blood-borne odorants.

That is, odors can "mask" trigeminal stimuli and vice versa. While masking does occur, the overall intensity of the experience is rated as more intense as the concentrations of the two stimuli increase. Stimulation of the nose and eye with low levels of odorous VOCs is often either additive or synergistic, leading to responses characteristic of irritants.


WALKER and colleagues have studied respiratory responses following stimulation of the eye and nose. Using a specially designed olfactometer that provided different channels for the eye and nose, they collected respiration data in human subjects to "nose only" and "eye + nose" trials.

Using amyl acetate (a banana-like and relatively pleasant smell at low concentration), they found that breathing flow rate increased at the lower concentration presented to "nose only." At the highest concentration of "nose only" administration, breathing flow was slightly reduced. When the same stimuli were presented to the "eye + nose," subjects responded as if they had been exposed to far more amyl acetate, that is, breathing was significantly reduced as a function of concentration.

From these studies, it appears that receptors in the eye interact with those in the nose to alter breathing and initiate respiratory volume reductions at relatively low concentrations of chemical stimulation.

The fact that odor sensations are linked so closely with irritant sensations is due in part to the central projections of the olfactory and trigeminal systems. The trigeminal nerve projects to fibers that overlap with brain areas of the olfactory projection such as the mediodorsal nucleus of the thalamus.

Additionally, the trigeminal nerve projects to many areas of the brainstem associated with autonomic responses such as nasal secretion, sneezing, and respiration.

Silver and Finger emphasized that these physiological reflexes are "among the strongest in the body." The magnitude of these responses underscores the evolutionary importance of olfaction as a warning and response mobilization system.


In addition, Cometto-Muniz and Cain found that thresholds for eye irritation closely predict nasal irritation thresholds, and can serve as a practical means to assess potency for nasal irritation in normosmics.


Electrophysiological methods for measuring responses to irritation include peripheral negative mucosal potentials (NMPs) and central event-related potentials (ERPs).


NMPs are recorded by means of an electrode on the septal wall of the nasal cavity along the line between bony and cartilaginous parts of the nose (referenced against the contralateral bridge of the nose). The NMPs are thought to result from activation of both C-fibers and A-delta fibers. -------

Reflexive changes in nasal blood flow to irritants can be measured using a laser Doppler flow meter. Pneumotachograph measurements indicate that there is a reduction of tidal volume (volume per breath) that begins at the threshold of nasal irritation. 

The RD50 (50% decrease in respiratory frequency) is calculated from the log concentration-response curve. A computerized version of this test has been developed to quantify breathing patterns in unanesthetized mice exposed to volatile chemicals.

It should be noted that reflex momentary apnea (interruption of inhalation) in response to irritation can also be recorded in humans. Apnea is reflexive response to irritant stimulation that protects the upper airway.

Breathing patterns before, during, and after presentation of various concentrations of a potential irritant can be used to determine the concentration sufficient to elicit the reflex.


While bioassays of irritation in animals can provide helpful information, current research suggests that humans are more sensitive to irritation than animals.


Historically, malodor has been considered an indicator of potential health risk. However, the mechanism by which unpleasant odors cause health complaints in the absence of irritation or toxicity is poorly understood. Health complaints do occur at levels of VOCs that are below irritant thresholds. -----

There is extensive animal literature that indicates that airborne chemicals can affect behavior. In humans, airborne chemical signals have even been shown to affect ovulation.


In one study, fourteen of 26 workers exposed to presumably safe levels of odorous sewer gases (as measured by gas detection equipment) experienced sore throat, cough, chest tightness, breathlessness, thirst, sweating, irritability, and loss of libido.

Severity of symptoms was dose related. Clinical follow up showed deteriorating respiratory symptoms and lung function tests in the most seriously affected.

Chemical analysis showed that the workers had been exposed to a mixture of thiols and sulfides. In another study, expose to the odor of n-propyl mercaptan in an agricultural setting for 6 weeks led to significant exposure effects including headache, diarrhea, runny nose, sore throat, burning/itching eyes, fever, hay fever attacks, and asthma attacks.

The mechanism by which these unpleasant odors induced health symptoms in the absence of irritation or toxicity is not know. However, Gift and Foureman reported that the RD50 values (concentration that induces 50% decrease in respiratory rate) for a random sample of unpleasant smelling compounds were much lower than for pleasant smelling compounds.

Schiffman found that shallow and irregular breathing patterns were induced by exposure to unpleasant odors (swine odors, rotten fish, SULFIDES) while deeper stable breathing patterns were characteristic of exposure to pleasant odors (chocolate chip cookies, orange cake). These differences in breathing patterns (whether genetic or learned) may influence health symptoms. -------

Electroencephalography (EEG) and functional magnetic resonance imaging (fMRI) studies have even shown that odorants and airborne chemicals can affect the nervous system without being consciously  detected.


Odors perceived to be unpleasant can impair mood and increase reactivity to startling stimuli. 

Negative mood, stress, and environmental worry can potentially lead to a number of physiological and biochemical changes with subsequent health consequences. These include elevations in blood pressure, both in normotensives and in patients with hypertension, immune impairment, increased levels of peripheral catecholamines, increased glucocorticoids, increased secretion of adrenocorticotropic hormone (ACTH) from the pituitary, decreased gastric motility, increased scalp muscle tension in patients with muscle tension headaches, and even hippocampal damage.

Chronic stress has been associated with development of coronary artery disease, chronic hypertension, and structural changes of the heart in some studies.

Thus, if odorous stimuli are sufficiently stressful, this could potentially elevate the catecholamines epinephrine and norepinephrine to levels that produce adverse cardiovascular effects including increased heart rate and blood pressure and increased tendency of blood to clot.



Odors can modify synaptic plasticity in the hippocampus and piriform cortex (parts of the limbic system) which are associated with learning and emotion. ----

Odor-conditioned panic attacks or panic disorder have been reported after exposure to odors in the workplace. Whether these learned responses should be deemed "health effects" from odors, however, is controversial because the term "health" has multiple meanings in scientific, regulatory, and legal settings.

According to the World Health Organization (WHO), the definition of "health" is "...a state of complete physical, mental, and social well-being and not merely the absence of disease or infirmity." Thus, a symptom that diminishes physical, mental, or social well -being would be a "health effect" according to WHO.

The majority of the participants at the Health Effects of Odors workshop considered it appropriate to explore health effects of odors within the WHO definition of health.

Participants at a subsequent workshop sponsored by the Centers for Disease Control also agreed the potential health effects associated with exposure to confined animal feeding operations (CAFOs) should be viewed according to the WHO definition of health.

Frist emphasized that reactions to odors such as nausea, headache, loss of sleep, and loss of appetite clearly represent a matter for public-health concern and attention under the WHO definition of health.

Using a broad definition of health that includes quality of life and social and mental well-being, Matchell et al concluded that malodorous air in an urban environment causes adverse health effects. ------



Odor intolerance has been associated with increased cardiopulmonary risk including increased sympathetic tone in the cardiovascular system at rest, different EEG alpha rhythms, lower rapid-eye-movement (REM) sleep, and greater prevalence of chronic cough, PHLEGM, wheeze, chest tightness, exertional dyspnea, acute respiratory illnesses, hay fever, child respiratory trouble, and physician confirmed asthma.

The reasons for these biological responses in odor-intolerant individuals are not known but mesolimbic systems could account in part for many of the cognitive, affective, and somatic symptoms.

Karol suggested that inhalation of airborne chemicals can augment allergic sensitization with episodic pulmonary reactions occurring on subsequent exposures. These reasons could involve the upper respiratory tract (rhinitis), lower respiratory tract (wheeze, bronchospasm), or systemic immune involvement (febrile response). While the mechanisms of sensitization are not well understood, mediators of immunity are definitely involved.


PAGES 31 - 32

In agricultural settings, odorant mixtures typically conain co-pollutants such as particulates, endotoxin, and pesticides. Particulates can arise from confinement building exhausts, dry feedlots, composting facilities, lagoons, and land application sprays. Particulates from intensive animal housing consist mainly of manure, dander (hair and skin cells), molds, pollen, grains, insect parts, mineral ash, feathers, indotoxin, and feed dust.

AIRBORNE DUST PARTICLES CAN CONCENTRATE ODORANTS SUCH AS ORGANIC ACIDS AND AMMONIA ON THEIR SURFACES; this contributes to odor potential and exacerbates irritancy induced by dust in the respiratory tract. Experimental studies have found a strong link between odor/irritation intensity and levels of particulates.

PARTICULATES ASSOCIATED WITH FECAL WASTE ARE ALSO KNOWN TO CARRY BACTERIA. Thus, it is likely that some of the health complaints ascribed to odor may, in fact, be caused by particulate matter (liquid or solid) suspended in air or by a synergistic effect between odorants and particulates.

A SYNERGISTIC EFFECT OF AMMONIA AND DUST EXPOSURE has been reported in a study of 200 poultry facilities. The adverse health effects of ammonia and particulates in combination was greater than the additive effect of ammonia and particulates by a factor of 1.5 to 2.0.

Both fine and coarse particles in an odorous plume enter the nasal cavity and can induce nasal irritation. However, these particles differ in the degree to which they traverse the respiratory tract.

Fine particles include particulate matter with sizes less than 2.5 uM (PM2.5). These particles are more likely than coarse particles to cause respiratory health effects because they reach the gas-exchange region of the lung.

Ultra-fine particles (i.e., those with a diameter 0.1 uM or less) may be even more toxic than larger sized particles producing severe pulmonary inflammation and damage and even affecting mortality.

Fine particles remain suspended in the atmosphere for days and can be transported thousands of miles. Particles with sizes from 2.5 uM to 10 uM (PM 2.5-10) are coarse particles that enter the thorax and may also induce health effects.

There is an overlap of fine and coarse mode particles in the intermodal region of 1 to 3 uM. Coarse particles are usually mechanically generated.

Sources of coarse particles near confined animal operations AND OTHER LOCATIONS OF BIOSOLIDS include windblown dust from soil, feed, manure, unpaved roads, pollen, mold spores, parts of plants and insects, and evaporation of aqueous sprays.

PAGES 32 -33

Fine particles may be formed in the atmosphere from gases through the processes of nucleation and growth. Nucleation entails formation of very small particles from gases.

Another example is the oxidation of NO2 to nitric acid (HNO3) which reacts with ammonia (NH3) to form fine particles of ammonium nitrate. Ammonia salts that exist as fine aerosols can be transported long-range in the atmosphere.

Third, photochemical reactions generate ozone and OH-, and these react with organic gases (such as odorous compounds) to form materials with low vapor pressure that can nucleate or condense on existing particles. ------

Epidemiologic studies of exposure to particulates have reported statistical associations between daily changes in health outcomes such as mortality and daily variations in the concentrations of different sizes of ambient particulate matter.

There is considerable epidemiological evidence predominantly from urban settings that exposure to increased levels of particulates is associated with increased mortality risk, especially among the elderly and individuals with preexisting cardiopulmonary diseases, such as chronic obstructive pulmonary disease (COPD), pneumonia, and chronic heart disease.

There is also epidemiological evidence that particulate exposure can increase the risk of respiratory and cardiovascular morbidity such as increased hospital admissions or emergency room visits for asthma or other respiratory problems, increased incidence of respiratory symptoms, or alterations in pulmonary function.


First, time-averaged sampling of dust downwind gives lower values than the peak dust levels because the samplers are usually in the plume for only a short period of time due to shifts in the wind direction.

Second, the geographical location where the plume reaches the level of potential perception e.g. a neighbor's nose) may be a small physical area that is difficult to locate for measurement purposes in real time.

Third, particulates from the swine confinement houses and particulates from the lagoon may both contribute to the exposure but may or may not occur simultaneously

BACTERIAL exposures e responsible for some health complains from exposure to odorous emissions from agricultural operations. Bacteria are ubiquitous in swine houses; furthermore, aerosols formed over lagoons may allow the transfer of bacteria from the water into the air with transfer downwind in aerosol droplets.

ENDOTOXIN, a heat-stable toxin associated with the outer membranes of certain gram-negative bacteria, can reach levels as high s 2,410 ng/m3 to 78,600 ng/m3 in swine facilities.

The American Conference of Governmental Industrial Hygienists' Threshold Limit Value-Time Weighted Average (ACGIH TLV-TWA for endotoxin is 10 ng/m3; that is the time-weighed average concentration for a conventional 8-hour workday and 40-hour workweek, to which nearly all workers may be repeatedly exposed daily without adverse effects.

ENDOTOXINS CAUSE AN INFLAMMATORY RESPONSE OF THE RESPIRATORY TRACT. Atopic asthmatic individuals have elevated sensitivity to respirable endotoxin which results in a variety of immune responses including increased eosinophils in the airways.


Furthermore, exposure allergens in atopic asthmatic individuals augments subsequent endotoxin-induced nasal inflammation

Studies that trace the transport of odorous VOCs within olfactory and trigeminal nerves may also be helpful in understanding health effects of odors.

Both small and large molecules can be transported to the brain in the olfactory and trigeminal nerves.


For example, herpes simplex virus can infect the trigeminal nerve and ultimately enter the CNS. VIRUSES can also infect olfactory receptor neurons. However, fare more research is needed to determine if any health effects from exposure to odorous emissions from agricultural facilities OR BIOSOLIDS are due to transport of VOCs of viruses in nasal sensory nerves.

Further research is also required to determine if the levels of dust, ENDOTOXIN, or other co-pollutants (such as flying insects) transported in odorous plumes are high enough to cause health symptoms in neighbors of agricultural or municipal operations.

Flying insects are attracted to odors from urine, feces and gut mucus and often follow odor plumes to find resources. Flying insects have the potential to carry disease.


Odors have been reported to exacerbate symptoms of asthma but it is not clear whether the main cause of this worsening is due to direct irritation of mucous membranes by the odorant, to sensory stimulation of the olfactory and/or trigeminal nerve, or to prior conditioning.

Asthma is characterized by bronchial hyper responsiveness and mucosal airway inflammation; it is the leading chronic illness among adults and children.

Epithelial damage and epithelial shedding occur in the airway passages in asthma as well as other respiratory disorders including nasal allergy and infantile wheeze.


Even healthy individuals exposed to a polluted environment (e.g. ozone) can experience epithelial shedding which can last up to 2 weeks or more. Nerve endings are exposed by epithelial shedding; this allows VOCs and particulates access to free nerve endings which augments irritation from inhaled pollutants. Irritants can then set up a low grade neurogenic inflammation with leukocyte recruitment that aggravates asthma and allergy. IT HAS BEEN SUGGESTED THAT EVEN ANAPHYLAXIS can be triggered by chemical odors.


There are health risks associated with prolonged exposure to highly odorous ambient air in the work or home environment. Persistent asthma-like symptoms can result from a single excessively high environmental or occupational exposure to odorous/irritant substances such as paint, floor sealant, AMMONIA, chlorine, acetic acid, and hydrogen sulfide from manure.

This syndrome was termed RADS (reactive airways dysfunction syndrome) by Brooks et al. The duration of the single exposure can be as short as a few minutes to as long as 12 hours.

RADS, by definition, occurs in persons with no evidence of preexisting pulmonary disease. Another defining characteristic is that symptoms can persist after termination of the exposure for at least three months; but in fact they may persist for one year or more.

Bronchial biopsies suggest respiratory epithelial injury, but the mechanisms operative in the syndrome appear to be nonimmunological. Persons with RADS were generally aware of an odor that was present during the irritant exposure.

Documented irritant odorant exposures include hydrogen sulfide, AMMONIA, and dust.


Chronic bronchitis, occupational (non-allergic) asthma, and non-infectious chronic sinusitis are also prevalent among pig farmers.

THESE SYMPTOMS CAN BE INDUCED BY ODOROUS AND IRRITANT VOCS AS WELL AS DUST AND ENDOTOXIN. There appears to be a synergistic effect between volatile compounds and dust exposure in producing these symptoms. Symptoms appear to be progressive with an annual decline in lung function.

Health symptoms can also occur acutely and reversibly with even brief exposure to odorous and dusty agricultural environments.


Workshop participants concluded that current evidence suggests that the symptoms complaints experienced by neighbors of some odorous animal operations AND OTHER SOURCES OF BIOSOLIDS may constitute health effects.

A set of potential study tools and biomarkers were proposed at the workshop to validate odor-related symptoms in clinical, epidemiologic, and research studies. These are given in Table 1. Workshop participants stressed the need to relate these health measures to levels of exposure.



Accurate methods to quantify odorous emissions are necessary to determine the relation between potential health symptoms and odors.

Furthermore there is wide variability among individuals in the odor intensities and odorant concentrations that cause health complaints.


While the acceptability of the odor of some VOCs depends on learned or cultural factors (experience), odors of other compounds such as H2S, MERCAPTANS, AMINES, and nitrogenous heterocylic compounds are considered offensive by most individuals.


One limitation with using GC/MS) (gas chromatography/mass spectrometry) to quantify odor is that the individual odorous compounds may not smell unpleasant at the concentrations in the mixture, yet the mixture (or combination of odorous compounds) may smell bad. Furthermore, the concentration of individual component compounds (or even concentration of total volatile organics) may not predict the level of odor potential.

A drawback to current E-nose (electronic nose) models, however, is that they are sensitive only in the high ppb or ppm range while the human nose has exquisite sensitivity in the ppt range



PAGES 43 - 44

Measurements of the number of particulates (as well as their odor quality) before, during, and after treatments can also be obtained in order to evaluate the amount of odor carried on particles (dust) compared to that carried in gaseous form.

Dust can be collected simultaneously on the farmer's property and on the neighbor's property using Andersen Non -Viable Eight-Stage Impactor Kits or other such devices.

These dust samples can be dissolved in water or other dilutent (e.g., just as dust dissolves in mucus) and evaluated for odor by the trained panel using static olfactometry.

Any odors from dust on the farmer's property may be compared to odors from dust on the neighboring property to determine if they come from the same source.

Levels of marker compounds such as AMMONIA and hydrogen sulfide can also be obtained at the houses, lagoon, property line, and at the neighbor's home. However, correlations between odor intensity and levels of hydrogen sulfide or ammonia have been inconsistent.

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In addition to animal operations, compost facilities are under increasing pressure to address odor emissions. Organic materials composted at such facilities include wastewater treatment residuals (BIOSOLIDS/SLUDGE), yard waste (grass, vegetables, SLUDGES, animal wastes (manures and carcasses), municipal solid wastes    (separated or unseparated), and industrial organics.

Odor emissions have been a factor in closure of several expensive compost facilities and are a significant obstacles to the implementation of composting as a waste management option in a number of locations.

PAGES 57 - 58


Our current state of knowledge clearly suggests that it is possible for odorous emissions from animal operations, wastewater treatment and recycling of biosolids to have an impact on physical health.

The most frequently reported symptoms attributed to odors include eye, nose, and throat irritation, headache, nausea, hoarseness, cough, nasal congestion, palpitations, shortness of breath, stress, drowsiness, and alterations in mood.

Many of these symptoms (especially irritation, headache, hoarseness, cough, nasal congestion, and shortness of breath) can be caused by stimulation of the trigeminal nerve in the nose at elevated levels of odorous VOCs.

Co-pollutants in an odorous plume may also play a role. A genetic basis for some odor aversions may be the basis for complains from unpleasant but nonirritating odors; unpleasant odors have been shown to activate different brain areas than pleasant ones.

Most published studies indicate that there are occupational health risks to workers in intensive livestock units who are exposed continuously to high concentrations of odorous VOCs, particulates, and microbes.

However, more scientific data are necessary to quantify health symptoms from the types of exposures experienced by neighbors downwind of livestock or wastewater operations (e.g. continuous exposure to the lower levels of odorous emissions or intermittent exposure to high levels from temporary discharges).

Objective scientific data must be obtained that relate specific concentrations of VOCs, particulates (including ammonium aerosols), and microorganisms alone and in combination to objective measures of health symptoms.

There are many potential study tools and biomarkers for the validation of odor-related health symptoms in clinical, epidemiological, and research studies (see Table 1).

These tools and biomarkers will be helpful in distinguishing between direct health effects (e.g. sensory irritation) and indirect effects (e.g. stress).

Objective measures of health effects must then be related to the concentrations of odorous emissions as well as frequency and duration of exposure. A variety of methods are available to quantify odorous emissions including olfactometry, gas chromatography, and the electronic nose. However, there is still a need to develop portable, reliable, and sensitive sensors for field measurement of odorous emissions in real time.

Future studies will help establish minimal risk levels (MRLs) for odorous emissions analogous to those utilized by the Agency for Toxic Substances and Disease Registry (ATSDR), that is, substance-specific minimal risk levels (MRLs) to evaluate health effects.

MRLs are defined as "estimates of daily human exposure to a chemical that are likely to be without an appreciable risk of adverse noncancer health effects over a specified duration of exposure."

In addition, knowledge of MRLs for odorous emission will assist in the development and implementation of cost-effective odor-abatement techniques that will enable operators of livestock and wastewater operations to meet performance standards.


(1) US EPA acknowledges in Appendix A of sludge Stockpiling Guide (available on line) that sewage sludge emits odor-causing gases including dimethyl sulfide, dimethyl disulfide, methyl mercaptan, trimethylamine and ammonia. OSHA, CDC, NIOSH, DOT, etc. all warn about serious health effects from inhalation of these toxic gases.

(2) 1999 Ecological Risk Assessment by Dowd, Gerba, Pepper and Pillai found that neighbors within 1640 feet of sludge-spraying operations are at high risk from " ...exposure to microbial pathogens from biosolids via aerosols."

Neighbors within 1640 feet of sludge stockpiles and landspreading operations are also at significant risk from bacteria from sludge aerosols, particularly if exposed to these airborne pathogens for over 8 hours with wind speeds 11 m.p.h.

(3) The National Institute of Occupational Safety and Health (NIOSH) has issued TWO Health Hazard Evaluations finding that sludge workers are exposed to airborne enteric bacteria and endotoxins from gram negative bacteria.  NIOSH says these pathogens are associated with gastrointestinal symptoms and illnesses which have been reported by sludge workers and others in close proximity to sludge sites.

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