94 In utero exposure to tobacco smoke

206

93

Abstracts

Indoor exposure to formaldehyde at concentrations below 50 ttg/m 3 does not contribute to asthma development.

J ALLERGYCLINIMMUNOL JANUARY 1996

95

P.G6rski. M.D. C Palczvfiski.M.D.J.Stankiewicz. M D . B.Ko~acifi.qka M D . - U R u t & M D . J.Gruchai& M D . A Krakowiak M D , B Szul¢ IVlD, J Jakubowski M D , W Hanke M D , Lbd~, Poland Some authorssuggestthatin peopleindoorexposedto formaldehydeatconcentration> 50 ttg/mathe frequencyof respiratoryallergyishigherthan in common population.The aim of the study was to evaluatetim exposureto formaldehyde as a facilitating factor of specific sensitization to commonallergens. 465 subjects, living in apartment houses that had been built 10 years before, participated in the study, Allergy was diagnosed with the use of questionnaire, total serum IgE level, skin prick tests with common allergens. Determination of formaldehyde was performed with a method based on reaction of aldehydes with dinitrophenylhydrazine. 98% of examined population were exposed to formaldehyde at classes of concentrations: 0-25 ttghn3 and 25-50 p.ghn~. There was no significant relationship between respiratory allergy occurrence and indoor exposure to formaldehyde at that concentrations. The results of the study suggest that formaldehyde at concentration below 50 I~g/m3 does not increase the occurrence of respiratory allergy.

94

In U t e r o Exposure to Tobacco Smoke. E Hossny MD~ A Hosni PhD~ R Mabrouk MD, Cairo, Egypt. To document the fetal exposure to maternal a c t i v e and passive smoking, 181 consecutive t e r m deliveries were enrolled in this study. According to maternal self report, the sample comprised 12 a c t i v e smokers, 97 passive smok~.rs (paternal smoking) and 72 nonsmokers. C o t i n i n e - the major nicotine m e t a b o l i t e was measured by ELISA in 102 cord blood samples to o b j e c t i v e l y v e r i f y the fetal exposure, The mean cord blood cotinine level of the 12 infants of smoking mothers (0.61+0.1 ug/ml) was significantly higher than that of 50 ] n ~ n t s of the group of passive smokers (0.39+0.13ug/ml, p<0.001) and of 40 infants of non-smoking mothers (0.24+0.13ug/ml, p<0.001). The l a t t e r s still had detectable amounts of cotinine (>0.01 u g / m l ) denoting significant exposure to nicotine despite the negative self reporting. Maternal a c t i v e smoking was associated w i t h significantly lower birth weight, length and skull circumference in the newly born babies while passive smoking was associated w i t h lower birth weights only and apgar scores as compared to neonates of non-smoking parents. Thus, Egyptian fetuses are a t risk of exposure to tobacco smoke and its hazards not only f r o m parental sources but also from exposure to environmental tobacco smoke(ETS). These data emphasize the need for nation-wide systematic persistant efforts to stop the exposure of pregnant women to tobacco smoke.

96

Formaldehyde and Respirable Suspended Particles L e v e l s in L o u i s i a n a H o m e s . R Lemus-Olalde MSc. TG Akers PhD. A Abdelghani ScD. New Orleans, LA Several studies have concluded that formaldehyde (HCHO) and Suspended Respirable Particles (RSP) are suspected of causing allergic respiratory diseases. With this in mind, a four season indoor air quality survey was undertaken in 52 homes found in eight Louisiana cities. HCHO samples were taken using XAD-2 adsorbent tubes treated with 2-(hydroximethyl) piperidine, and analyzed later with gas chromatography. RSP levels were measured using an aluminum cyclone (cutpoint= 5 p.m) with a 37-ram cassette filter (pore size = 0.45~m), followed by gravimetric determination. For the spring sample the average HCHO level was 0.26 ppm (s.d.= 0.22); with a maximum of 1.03 ppm and a minimum of 0.01 ppm. Forty houses out of 52 (77%) exceeded the American Society of Heating, Refrigerating, and Air-Conditioning Engineers (ASHRAE) guideline of 0.1 ppm. The mean level of RSP was 0.25 mg/m3 (s.d. = 0.45); with values ranging from non-detectable to 3.13 mg/m3. Of all the houses, 58% exceeded the 24 hr California PMw Standard of 50 pg/m3. These results suggest that some of these houses do not afford enough protection to sensitive persons or asthmatics from HCHO and RSP.

Mechanism

of Persistent Inflammation

in R A D S

and RUDS. YYJ_~oo¢ UP: T Fl~hAikh MD= W I M~tTaAr Mr) M Albums7 Mr): R I~lnr.h MD, Greenville, NC RADS is a chronic asthma-like condition developing after an acute inhalation exposure to smoke, dust, or fumes. RUDS is chronic irritant rhinitis with a toxic inhalation exposure. The pathophysiology of this chronic inflammation is unknown. A study of the ultrastructure of biopsies of the nasal mucosa in patients with these syndromes developing in temporal association with a CIO2 exposure was undertaken, to see if a basis for the persistent rhinitis could be determined. Specimens from 13 individuals who developed RADS and/or RUDS after occupational exposure to CIO2 were studied, along with 3 nonexposed control subjects. Formalin fixed specimens stained with H&E and immunoperoxidase stains for S-100 (nerve fibers) revealed chronic inflammation with lymphocytic infiltrates and proliferation of nerve fibers in patients vs. controls (p< 0.05). Glutualdehyde fixed specimens examined by electron microscopy showed descluamation of the epithelium and permeability of epithelial cell junctions in patients but not controls, similar to that resulting from tumor necrosis factor. These findings suggest a mechanism for the persistent airway inflammation resulting from a toxic inhalation. Subsequent low level irritant exposures can permeate epithelial cells to reach sensory nerves, producing neurogenic inflammation. The chronic lymphocytic infiltrates may result in tumor necrosis factor release, producing epithelial cell permeability. The proliferation of nerve fibers by an undetermined factor further enhances response to irritants,