Chronic Exposure to Sulfur Dioxide

Scanlon, Paul D.; Seltzer, Janet; Ingram, R. H.; Reid, Lynne; Drazen, Jeffrey M.

doi:10.1164/arrd.1987.135.4.831

Cited by 25 publications

(1 citation statement)

References 30 publications

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“…Inflammation of the lower airways -known to follow S 0 2 exposure in animals [10] -probably plays an impor tant role in allergic sensitization. Permeability of the epi thelium has been shown to be increased in inflamed air ways in both animals [11] and man [12], leading to in creased contact of the antigen with bronchus-associated lymphoid tissue.…”

Section: Discussionmentioning

confidence: 99%

SO<sub>2</sub>-Induced Enhancement of Inhalative Allergic Sensitization Inhibition by Anti-Inflammatory Treatment

Riedel¹,

Naujukat²,

Rüschoff

et al. 1992

Int Arch Allergy Immunol

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Epidemiological studies have shown a relationship between air pollution and allergic airway disease. In a previous study we have found that exposure to SO₂ enhances allergic sensitization to inhaled ovalbumin (OA) in the guinea pig. We have now investigated the influence of pre-treatment with anti-inflammatory drugs on SO₂-induced enhancement of allergic sensitization in this model. Four groups of 6 guinea pigs each were exposed to 5 ppm SO₂ on 5 consecutive days over 8 h per day with intermittent inhalation of OA, while the air-control group was exposed to clean air and OA. During the period of SO₂ exposure and sensitization three experimental groups were treated with indomethacin (group I), methylprednisolone (group M) and nebulized nedocromil sodium (group N), while the control group remained untreated. Guinea pigs were investigated for sensitization to OA by specific bronchial provocation tests using body plethysmographic measurement of compressed air (CA) and by measurement of specific antibody response in serum. While in the SO₂-exposed control group 5 of 6 animals reacted to specific bronchial provocation testing (CA median 0.15 ml, range 0-0.175 ml), only 1 animal was sensitized in group M (CA 0 ml, 0–0.125, p < 0.05), whereas no bronchial reactions were seen in groups I and N (CA 0 ml, 0–0.05, p < 0.025). Specific IgG antibody titres increased in the control group (median 43 EU → 85 EU), but not in the treatment groups (medians group 135 EU → 35 EU, group M 30 → 35 EU, group N 64 → 50 EU). We conclude that anti-inflammatory treatment with methylprednisolone, indomethacin or nebulized nedocromil sodium during the period of SO₂ exposure inhibits SO₂-induced enhancement of inhalative allergic sensitization in our guinea pig model.

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Section: Discussionmentioning

confidence: 99%