Aerosol exposure

Norwood, D. M., Wainman, T., Lioy, P. J., and Waldman, J. M. (1992). Breath ammonia depletion and its relevance to acidic aerosol exposure studies. Arch, of Fa-wtron. Health 47, 309-313. 

Delayed. Usual onset of symptoms occurs approximately 2 h after aerosol exposure. Depending on inhaled or ingested dosage, symptoms may appear at times ranging from 30 min to 20 h after exposure. Effects from skin contact may appear 36 h later. Dimethylsulfoxide as a "carrier" increases the percutaneous effect by a factor of at least 25. 

In general, intraperitoneal and intravenous injections were the most sensitive administration routes (Bauer 1983). LD50 dermal values, however, are often not true percutaneous values because of oral contamination from normal grooming (Summers 1980). Aerosol exposure to paraquat produced a concentration-dependent rapid, shallow breathing pattern in guinea pigs (Cavia sp.)... 

Aerosol exposure, in mg/m3 0.1, 0.4, or 0.8, 6 h daily, 5 days weekly, 3-week exposure Rapid shallow dose-dependent breathing pattern, with return to control values during first 7 days of exposure, suggesting adaptation (Burleigh-Flayer and Alarie 1988)... 

Differential Diagnosis An epidemic of inhalation anthrax in its early stage with nonspecific symptoms could be confused with a number of viral, bacteria, and fungal infections. Progression over two to three days with sudden development of severe respiratory distress followed by shock and death within twenty-four to thirty-six hours in essentially all untreated cases eliminates diagnosis other than inhalation anthrax. Other diagnosis to consider would include aerosol exposure to staphylococcal enterotoxin B (SEB), plague, or tularemia pneumonia. 

Vaccine Efficacy (for aerosol exposure)/antitoxin Currently no human data. Persistency Spores are highly stable. 

Caution Although there is a vaccine for anthrax exposure, there is currently no human data for aerosol exposure. 

Vaccines Yes (Greer Laboratory Vaccine). A licensed, killed vaccine is available. Initial dose followed by a second smaller dose one to three months later, and a third dose three to six months later. A booster dose is to be given at six, twelve, and eighteen months and then every one to two years. Please Note This vaccine may not protect against aerosol exposure. Live-attenuated vaccines are available outside the United States, but they tend to be highly reactogenic and without proven efficacy when challenged with aerosol dissemination. 

Prophylaxis For asymptomatic patients exposed to plague aerosol, or to a patient with suspected pneumonic plague, provide doxycycline at 100 mg orally twice daily for seven days, or for the duration of risk of exposure plus one week. Alternative antibiotics include ciprofloxacin, tetracycline, or chloramphenicol. No vaccine is currently available for plague propylaxis. The previously available licensed, killed vaccine was effective against bubonic plague, but not against aerosol exposure. 

Signs and Symptoms Weakness, fever, cough, and hypothermia about thirty-six hours after aerosol exposure, followed in the next twelve hours by hypotension and cardiovascular collapse. 

Caution Ricin is extremely toxic to cells and acts by inhibiting protein synthesis. After aerosol exposure, signs and symptoms would depend on the dose inhaled. Humans can be expected to develop severe lung inflammation with progressive cough, dyspnea, cyanosis, and pulmonary edema. 

Signs and Symptoms From three to six hours after aerosol exposure, sudden onset of chills, fever, headache, pain in one of more muscles, and nonproductive cough. Some patients may develop shortness of breath and retrostenal (situated or occurring behind the sternum) chest pain. Fever may last two to five days, and cough may persist for up to four weeks. Patients may also experience nausea, vomiting, and diarrhea if they swallow toxin. Higher exposure levels can lead to septic shock and death. 

Chemical Substance A substance usually associated with some description of its toxicity or exposure hazard, including solids, liquids, mists, vapors, fumes, gases, and particulate aerosols. Exposure, via inhalation, ingestion, or contacts with skin or eyes, may cause toxic effects, usually in a dose-dependent manner. 

Knott, M. J., and M. Malanchuk. Analysis of foreign aerosol produced in NOa-rich atmospheres of aerosol exposure chambers. Amer. Ind. Hyg. Assoc. J. 30 147-152, 1%9. 

Heart muscle degeneration was reported in mice exposed to 50 mg/m of o-cresol 2 hours/day for 1 month (Uzhdavini et al. 1972). The cresol was probably given as an aerosol. Exposure levels were not reliably documented. 

In 1955, 12 subjects underwent up to 14 aerosol exposures of 45 min each. The maximal cumulative Ct was 30,800 mg-min/m. Ten subjects sustained dermal effects and discontinued the test after eight to twelve exposures. Erythema occurred on trunks and extremities. Three subjects had blisters. One subject, whose total Ct was 17,700 mg-min/m, was hospitalized 5 d after his last exposure because of diffuse erythema and bullae. ... 

In another 1963 experiment, 13 subjects underwent up to 10 aerosol exposures of 15-60 min each. The maximal cumulative Ct was 16,000 mg-min/m. There were no injuries. 

In 1973, Upshall4 reported tests of CS for teratogenicity in female Porton strain rats and New Zealand White rabbits. He attempted to simulate conditions that exist in riot-control situations, looking for teratogenesis and changes in numbers of offspring in response to aerosol exposure of both species. Control rats were subjected to handling stress and aerosols without CS. 

Aerosol exposures were at 6, 20, and 60 mg/rn for 5 min on days 6-13 of pregnancy in rats and days 6-18 of pregnancy in rabbits. Control aerosols consisted of water or suspensions of Neosil (silica dust), and the experiments were conducted with 12-24 animals. The adults were killed a day before parturition rat fetuses were examined for 18 abnormalities and rabbit fetuses for eight abnormalities. In addition, rats were studied for teratogenic effects after exposure to CS by intraperitoneal injection at 20 mg/kg on day 6, 8, 10, 12, or 14 of pregnancy. 

From 1958 to 1973, at least 1,366 human subjects underwent experimental exposures to CS at Edgewood. For 1,073 subjects, there was some type of aerosol CS exposure, 180 subjects had skin applications, 82 subjects had both skin applications and aerosol exposures, and 31 underwent CS applications to their eyes. 

Between 1958 and 1972, 99 human subjects underwent experimental exposures to CN at Edgewood Arsenal. Sixty-nine subjects had aerosol exposures in a chamber that they entered masked they removed the masks after the agent concentration had equilibrated. Thirty subjects had direct skin applications of CN. 

Exposure data are available on 68 of the 99 subjects 16 had one to five aerosol exposures in 1958, 44 had one to three aerosol exposures in 1965, and eight had one dermal application in 1968. No exposure data are available on the other 31 subjects nine had one... 

The only dosage Information on the sixteen 1958 aerosol-exposure subjects Is exposure time, which was recorded on seven of the subjects and ranged from 0.32 to 3.63 min. The 44 subjects who underwent aerosol exposures In 1965 experienced Ct s of 6-315 mg mln/m and exposure time of 0.15-3 min. The eight dermal- exposure subjects In 1968 had 0.01-0.025 ml of CN applied to their bare or clothed arms. 

The effects on the aerosol-exposure subjects were transient, generally resolving within minutes of removal of the agent. There also seemed to be tolerance In experienced subjects, often Increased by closing the eyes. Predominant effects of aerosol exposure were ocular lacrlmatlon, blepharospasm, conjunctivitis, and, rarely, palpebral edema. Respiratory effects of aerosol exposure were nasopharyngeal Irritation, rhlnorrhea, and, rarely, dyspnea. Skin Irritation was prominent on shaved areas. Other rare effects of aerosol exposure were headaches and dizziness. No laboratory analyses were recorded for aerosol exposure. 

From 1963 to 1972, 97 subjects underwent experimental exposures to CR at Edgewood 33 had aerosol exposures In a chamber, and 64 had cutaneous exposures. 

Several CR subjects exposed In the aerosol chamber commented that CR was milder than "tear gas. The effects of exposure to CR aerosol were transient and predominantly respiratory and ocular. All subjects with aerosol exposures had upper respiratory tract Irritation with choking. Many subjects had dyspnea some were tachypnelc. Ocular irritation from aerosol exposure was common, often causing blinking, closing of the eyes, and lacrlmatlon and Interfering with the subject s ability to carry out simulated battlefield functions. 

Inhalation toxicity Aerosol exposure (mass median diameter, 1.8 um) produced similar toxic signs In rats, mice, and guinea pigs. 

In 1972, 21 subjects underwent exposure to CS815799. Seven subjects had aerosol exposures at a Ct of 50 mg-mln/m one was exposed twice. CS815799 exposure caused mild ocular and respiratory Irritation. laboratory analyses 7 d after exposure revealed Increased SGOT (43.8 and 42.7 IU) In two subjects, both of whom had normal pre-exposure SGOT. One of these two subjects also had 6-10 white cells in urinary sediment—a finding not seen In preexposure urinalysis. 

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