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Litigation issues

Hydrogen sulfide as an odor nuisance:

Easily detectable levels of this gas are commonly found in the vicinity of waste lagoons, geothermal facilities, special waste disposal sites, petrochemical installations, volcanic activity, and the like. In the experience of the author, industrial emissions of hydrogen sulfide gas that initiate litigation rarely reach as high as 0.100 ppm and are usually much lower. At air concentrations of 0.250-0.300 ppm, the odor of hydrogen sulfide, especially if frequent or persistent, can create a nuisance problem of legitimate concern. Accordingly, under some conditions, complaints of headache and sleep disturbances attributed to hydrogen sulfide emissions may be well founded. It is important to emphasize that there is no reliable evidence that intermittent exposure to air levels less than a few ppm does causes physical illness, long-term health effects, or hypersensitivity to other chemical substances.

Hydrogen sulfide exposure with symptoms

Mild, transitory symptoms of exposure such as headache, dizziness, and incoordination can appear within seconds to minutes following exposure to several hundred ppm of hydrogen sulfide gas. At higher levels, symptoms can include abrupt collapse with or without apnea.

For the purposes of clarification, acute hydrogen sulfide neurotoxicity characterized by sudden collapse and loss of consciousness can be considered in three increasingly severe stages (Milby and Baselt, 1999b):

Stage One: Sudden collapse followed by prompt and complete recovery.
The victim continues to breathe and the heart continues to beat. There are no lasting effects.
The phenomenon referred to in the medical literature as "knockdown" is included in this category.
Stage One appears to be the most common form of hydrogen sulfide-induced collapse.

Stage Two: Sudden collapse with delayed recovery.
Spontaneous breathing continues. Most victims recover completely, but a few develop sequelae
ranging from minor neurological deficits to major, debilitating dementias.

Stage Three: Sudden collapse and prolonged unconsciousness with respiratory paralysis and
apnea leading to hypoxic encephalopathy.
Only a few cases of acute hydrogen sulfide intoxication can be considered as Stage Three.
Delayed rescue or exposure to concentrations of hydrogen sulfide gas exceeding 1500 ppm are
often factors contributing to Stage Three collapse.

To be exposed to hydrogen sulfide is not necessarily to be damaged by it. Hydrogen sulfide, when inhaled, is very rapidly destroyed by the blood and does not accumulate in the body. Accordingly, although repeated exposures to small concentrations of this gas may be understandably considered a nuisance, such exposures are of no toxicological significance. Recovery from hydrogen sulfide poisoning is nearly always complete if apnea or other causes of respiratory insufficiency such as pulmonary edema or airway obstruction did not enter the picture. After recovery, there is no relapse.

SULFUR DIOXIDE

Sulfur dioxide fumes are not absorbed into the body and do not penetrate through the skin. The toxic effects of sulfur dioxide are derived wholly from its ability to directly irritate the eyes, the moist mucous membranes of the upper respiratory tract, and the lung. Acute impairment of lung function associated with toxicologically significant exposure to sulfur dioxide is obstructive in nature due, at least in part, to irritant-induced bronchoconstriction.

Controlled studies in humans have documented that acute inhalation of sulfur dioxide can cause bronchoconstriction, particularly in asthmatics. As a group, exercising asthmatics are probably the persons most susceptible to sulfur dioxide inhalation, often responding adversely to levels of 0.1 ppm (PHS, 1998). Among healthy volunteers, the threshold for respiratory function changes is about 1.0 ppm over a period of several hours. These acute functional changes, reflex-mediated bronchoconstriction, tend to disappear during exposure or shortly thereafter (Merchant, 1986). It is not clear whether adaptation to these low concentrations takes place with repeated exposure, although workers exposed to sulfur dioxide on a daily basis appear to develop some tolerance to its irritating effects (Keogh, et al., 1932; Romanoff, 1939; Greenwald, 1954).

The characteristic "burning match" odor of sulfur dioxide is detectable by most persons at air concentrations of about 0.5 ppm. At levels of 10-20 ppm, nose, throat, and upper respiratory track irritation become prominent complaints. Eye irritation is not an early symptom and often becomes apparent at 10 and 50 ppm (PHS, 1998). Accidental exposure to 100 ppm for a few minutes has caused serious bronchitis (Skalpe, 1964).

Because of its irritating characteristics, persons exposed to sulfur dioxide at air concentrations of more than a few ppm will make every effort to "flee the scene". Accordingly, as a practical matter, only persons who cannot promptly evacuate an area contaminated by sulfur dioxide are at significant risk of incurring non-trivial injury to the eyes or respiratory tract.

A 10-year follow-up study of workers exposed to sulfur dioxide air concentrations ranging from 4 to 33 ppm did not reveal an increase of chronic respiratory disease or deterioration of pulmonary function as compared to a control group (Ellenhorn and Barceloux, 1988).

A biphasic response to exposure to very high concentrations of sulfur dioxide has been described (Weiss, 1994; Woodford, et al, 1979; Rabinovitch, et al., 1989; Charen, et al., 1979; Galea, 1964). The first phase consists of immediate symptoms of eye, nose, and throat irritation with chest tightness and non-productive cough. The second phase, appearing several weeks later, is characterized by respiratory failure due to fibrosis of the terminal bronchioles (bronchiolitis obliterans).

Sulfur dioxide exposure and reactive airway dysfunction syndrome (RADS)

In 1985, Brooks and his colleagues described an asthma-like illness in men who had undergone a single inhalation exposure to high levels of an irritating vapor, fume, or smoke (Brooks, et al., 1985). The investigators termed this illness "reactive airway dysfunction syndrome (RADS)". None of the affected individuals had preexisting respiratory disease and, following exposure, all showed positive methacholine challenge tests. Brooks and his colleagues established eight clinical criteria for the diagnosis of RADS: 1. Documented absence of preceding respiratory complaints; 2. Onset of symptoms after a single, specific exposure; 3. Exposure was to an irritating gas, smoke, fume or vapor present in very high concentrations; 4. Onset of symptoms within 24 hours after exposure and persisting for least three months; 5. Symptoms were asthmatic in nature; 6. Pulmonary function test may show airflow obstruction; 7. Methacholine challenge testing was positive in every case; and 8. Other types of pulmonary diseases were ruled out.

Since Brooks, et al reported their original diagnostic criteria for RADS, additional observations have been reported by Brooks and others that have substantively modified these diagnostic criteria. The most significant of these modifications include: 1. Descriptions of patients diagnosed with RADS whose exposure to workplace irritants was not limited to a single incident, but who experienced exposures to irritants at work for over six months before onset of symptoms. They were working when diagnosed, but were unable to relate the onset of their respiratory symptoms to any given accident or unusual event at work (Tarlo and Broder, 1989); 2. A report by Cone, et al. (1994) describing the first appearance of RADS fully a week after an accident involving a number of individuals exposed to a respiratory irritant ; 3. A report by Kipen, et al. (1994) describing a number of cases of low-dose RADS in whom symptoms developed following repetitive exposures to low doses of irritants; and 4. A report by Brooks, et al. (1998), describing a series of cases of "not-so-sudden-onset" irritant-induced asthma, characterized by exposures that were neither massive nor single.

High-level exposure to sulfur dioxide has been reported to cause airway hyperreactivity consistent with RADS (Harkonen, et al., 1983; Alford, et al., 1988; Pilirili, et al., 1996).

Litigation Issues

In the author's experience, brief exposure to about 5-ppm sulfur dioxide can precipitate an acute asthma attack in a person with preexisting asthma. The author is not aware of any reliable scientific evidence that low level exposure to sulfur dioxide, whether single or repeated, can cause asthma in a previously non-asthmatic individual.

The term RADS, in the author's experience, is used frequently and often imprecisely to describe a host of pulmonary problems that bear little or no relationship, either clinically or etiologically, to the syndrome describe by Brooks and his colleagues and later modified by other competent clinical investigators. The differential diagnosis of RADS includes, but may not be limited to acute tracheobronchitis, vocal cord dysfunction syndrome, gastrointestinal reflux disorder, and hypersensitivity pneumonitis.