Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study determined exposure-response relationships to side-stream tobacco smoke (2 hrs; 0, 1, 5, and 15 ppm CO) in 29 healthy nonsmoking young adults. Sixteen subjects had no history of environmental tobacco smoke rhinitis (ETS-NS) while 13 subjects had a history of ETS rhinitis (ETS-S). Eye irritation and odor perception showed a statistically significant exposure response in both groups; headache was significant in ETS-S and nose irritation was significant in ETS-NS subjects. Significant postexposure (P1) symptoms were first reported at 1 ppm CO among both groups, but in 3/9 symptoms were significantly greater at this exposure level in ETS-S subjects. Nasal congestion, rhinorrhea, and cough increased significantly at 15 ppm CO only. In ETS-S subjects, nasal volume decreased and nasal resistance increased in an exposure-response fashion. ETS-NS subjects had a qualitatively different shape to the exposure-response curve; significant dimensional reductions in mid- and posterior nasal volume occurred with exposure at 1 ppm CO but not at 5 ppm CO and reductions in posterior nasal volume occurred at 15 ppm CO exposure. These studies indicate subjective and objective response relationships with exposure to sidestream tobacco smoke at concentrations from 1 to 15 ppm CO. Some differences are noted among the two subject groups in the magnitude of some symptoms at the lowest exposure level and in the qualitative shape of the acoustic rhinometry and nasal resistance exposure-response curves.
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PMID:Tobacco smoke upper respiratory response relationships in healthy nonsmokers. 883 43

The purpose of the study was to test the hypothesis that infants with higher levels of prenatal exposure to polycyclic aromatic hydrocarbons (PAHs) from fossil fuel combustion may be at greater risk of developing respiratory symptoms. The study was carried out in a cohort of 333 newborns in Krakow, Poland, followed over the first year of life, for whom data from prenatal personal air monitoring of mothers in the second trimester of pregnancy were available. The relative risks of respiratory symptoms due to prenatal PAHs exposure were adjusted for potential confounders (gender of child, birth weight, maternal atopy, maternal education as a proxy for the socio-economic status, exposure to postnatal environmental tobacco smoke, and moulds in households) in the Poisson regression models. Increased risk related to prenatal PAH exposure was observed for various respiratory symptoms such as barking cough (RR = 4.80; 95% CI: 2.73-8.44), wheezing without cold (RR = 3.83; 95% CI: 1.18-12.43), sore throat (RR = 1.96; 95% CI: 1.38-2.78), ear infection (RR = 1.82; 95% CI: 1.03-3.23), cough irrespective of respiratory infections (RR=1.27; 95% CI: 1.07-1.52), and cough without cold (RR = 1.72; 95% CI: 1.02-2.92). The exposure to PAHs also had impact on the duration of respiratory symptoms. The effect of PAHs exposure on the occurrence of such symptoms as runny nose or cough was partly modified by the simultaneous exposure to postnatal passive smoking. The analysis performed for the duration of respiratory symptoms confirmed significant interaction between PAHs exposure and postnatal ETS for runny or stuffy nose (RR = 1.82; 95% CI: 1.57-2.10), cough (RR = 1.18; 95% CI: 0.99-1.40), difficulty in breathing (RR = 1.39; 95% CI: 1.01-1.92) and sore throat (RR = 1.74; 1.26-2.39). Obtained results support the hypothesis that prenatal exposure to immunotoxic PAHs may impair the immune function of the fetus and subsequently may be responsible for an increased susceptibility of newborns and young infants to respiratory infections.
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PMID:Prenatal ambient air exposure to polycyclic aromatic hydrocarbons and the occurrence of respiratory symptoms over the first year of life. 1617 Jun 61