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Results for “Sulfur Dioxide”

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At least 19 recordsLinked to original sources

PubMedDate not supplied

Effects of ozone and sulfur dioxide on virus growth in mice.

Inhalation of ozone and sulfur dioxide inhibited influenza virus growth in the nose of mice. Ozone inhalation caused the more pronounced inhibition of influenza virus growth: 0.6 ppm ozone for 3 hours post-virus exposure almost completely inhibited influenza virus growth in the nose, whereas sulfur dioxide (6 ppm for 7 days) causes only partial inhibition of influenza growth in the nose. Neither gas altered the propagation of influenza virus in the lungs of mice. Vesicular stomatitis virus (VSV) growth was either unaffected by exposure to ozone (0.9 ppm for 3 hours) or, when ozone exposure preceeded VSV exposure, the virus may have grown to slightly higher titer. The inhibitory effect of ozone and sulfur dioxide on influenza virus growth in nasal epithelium suggests a competitive interaction between the chemical inhalant, the virus, and host tissues, with net consequences for the pathogenesis of this disease. If the effcts of these inhalants are to be properly interpreted, they should be determined for all major regions of virus growth and inhalant deposition.

Animals↗

PubMedDate not supplied

Human exposure to sulfur dioxide and ozone: absence of a synergistic effect.

Studies of the human health effects of exposure to a combination of ozone and sulfur dioxide have produced somewhat conflicting results; the possibility of a synergistic enhancement of toxicity when the two gases are present simultaneously remains equivocal. We evaluated the effects of 0.40 ppm sulfur dioxide, 0.40 ppm ozone, and the combination of these two under one environmental condition (25 degrees C and 45% relative humidity). Subjects alternately walked and rested during a 2-hr exposure. Subjects exposed to filtered air or to 0.40 ppm sulfur dioxide showed no significant changes in pulmonary function. When exposed to either ozone or ozone plus sulfur dioxide, significant decreases in maximum expiratory flow, forced vital capacity, and inspiratory capacity were observed. There were no significant differences in response between ozone alone and ozone plus sulfur dioxide exposures, thus, in our subjects on synergistic effects were discernible.

Adolescent↗

PubMedDate not supplied

Effect of near ambient exposures to sulfur dioxide and ferrous sulfate particles on murine pulmonary defense mechanisms.

An infectivity model was used to test the safety margins for presently established air quality standards for sulfur dioxide and sulfate particles. Mice and rats were exposed to atmospheres of sulfur dioxide and mono-disperse ferrous sulfate particles from 3 to 6 times the standard for 17 hr prior to, or 4 hr after infection with aerosols of Staphylococcus aureus or Group C Streptococci. Exposure to these concentrations of pollutants did not impair the rodents' ability to ingest and inactivate the minimally virulent Straphylococcus or enhance the virulence of the Group C Streptococci. Insofar as these results can be extrapolated to man, the present air quality standards for sulfur dioxide and sulfate particles are protective in regard to respiratory bacterial infection.

Aerosols↗

PubMed1979

Effect of oil mists on the irritancy of sulfur dioxide. I. Mineral oils and light lubricating oil.

The increase in pulmonary flow resistance in unanesthetized guinea pigs was used to assess the effect of sub-micrometer oil aerosols on the response to sulfur dioxide. At a concentration of about 10 mg/m3 neither a medicinal grade mineral oil nor a light lubricating oil altered the response when given simultaneously with 1 or 10 ppm sulfur dioxide. The naphthenic medicinal oil at 100 mg/m3 failed to protect against 50 ppm sulfur dioxide when administerd simultaneously. A 30-minute pre-exposure, however, conferred complete protection. A paraffinic laboratory grade mineral oil conferred protection when given simultaneously but was less effective when the pre-exposure protocol was used.

Aerosols↗

PubMed1979

Pulmonary injuries associated with acute sulfur dioxide inhalation.

This report describes an industrial accident in which 5 previously healthy persons were acutely exposed to very high concentrations of sulfur dioxide. Of these 5 subjects, the 2 with the highest exposure died immediately; histologic examination of the lungs revealed extensive sloughing of the mucosa of large and small airways along with hemorrhagic alveolar edema. The 3 survivors were evaluated with pulmonary function tests performed at regular intervals. One subject subsequently developed symptomatic severe airway obstruction unresponsive to bronchodilators; another subject developed asymptomatic mild obstructive and restrictive disease, and the third subject continued to be asymptomatic with normal pulmonary function tests. This report severe to document the histologic features of fatal exposure to sulfur dioxide and stresses the need to follow parameters of pulmonary function in the nonfatal cases.

Accidents, Occupational↗

PubMed1977

Stability of patulin to sulfur dioxide and to yeast fermentation.

The affinity of patulin for sulfur dioxide (SO2) is much less than was previously reported and is of little significance at the SO2 concentrations (below 200 ppm) used in the processing of apple juice and cider. However, at concentrations of 2000 ppm SO2 and 15 ppm patulin, combination was 90% complete in 2 days. Removal of SO2 liberated only part of the patulin, which suggests that 2 mechanisms are involved: one reversible (opening the hemiacetal ring) and one irreversible (SO2 addition at the double bond). Test with 2 yeasts used in English commercial cider making confirmed that patulin is effectively removed during yeast fermentation.

Chemical Phenomena↗

PubMed1979

Embryotoxicity of inhaled sulfur dioxide and carbon monoxide in mice and rabbits.

The embryotoxic and teratogenic potential of sulfur dioxide (SO2) was evaluated in CF-1 and New Zealand rabbits exposed to SO2 alone or in combination with carbon monoxide (CO). The animals inhaled filtered room air (controls), SO2 (mice, 25 ppm; rabbits, 70 ppm), or SO2 plus CO (250 ppm) for 7 hr/day from days 6 through 15 (mice) and from days 6 through 18 (rabbits) of gestation. In both species, inhalation of SO2 resulted in slight toxicity in the dams and an increased incidence of minor skeletal variants among their offspring; exposure to the combination did not potentiate the increased incidence of these variants. A teratogenic effect was not discerned in either mice or rabbits exposed to SO2 alone or in combination with carbon monoxide, but the fetuses of mice exposed to the combination were significantly smaller than those exposed only to SO2.

Abnormalities, Drug-Induced↗

PubMed1979

Obstructive lung disease from acute sulfur dioxide exposure.

A previously healthy, non-smoking young man is presented who was briefly exposed to a high concentration of sulfur dioxide. An immediate episode of pulmonary edema was followed by a silent interval with subsequent development of a severe, irreversible obstructive syndrome. This history, together with radiographs showing hyperinflation and sequential physiologic studies indicative of obstruction without bronchospasm and without loss of parenchyma suggest bronchiolitis obliterans as the causative lesion. The literature concerning this syndrome and its relationship to toxic inhalation is briefly reviewed.

Adult↗

PubMed1977