RESUMO
Diverse environmental exposure profiles exist in the Americas because of widely different climates, ambient pollutants, and bioaerosols in these continents. This paper reviews selected studies from the Americas that support the broad hypothesis that environmental factors contribute to respiratory hypersensitivity. Processes influenced by environmental factors include primary immunologic sensitization, the development and exacerbation of specific immunologic diseases and the activation of nonspecific mechanisms with tissue inflammation, injury and remodeling. Endpoints resulting from these processes include respiratory symptoms, diseases such as asthma, with measures of disease severity including medication use and hospitalization rates, and death due to cardiorespiratory disease. Studies associate sensitization rates to specific allergens with environmental factors such as humidity and indices of allergen exposure. Regional variation occurs with exposure to outdoor source pollutants such as ozone, but varies by household to bioaerosols such as dust mite, cat or cockroach allergen. Indoor allergens are associated with asthma while outdoor allergens are associated with allergic rhinitis. In a national survey, the atopic sensitization rate in the USA increased with urban residence (defined as towns of population > 2500) and varied by region. Controlled human challenge studies show that ozone increases the response of allergic subjects to allergen. Increased ambient photochemical pollution concentrations, of which ozone is an important component, are associated with increased emergency room visits for asthma in cities such as Toronto, New York, Atlanta, and Mexico City. In Sao Paolo, Brazil, mortality due to childhood respiratory disease was influenced by the ambient levels of NO2. Epidemiologic studies including the recent meta-analysis of a large, longitudinal study population associate ambient concentrations of particulate matter < 10 microns and respiratory symptoms, disease severity and increased cardiorespiratory deaths. Toxicology studies show that individual variation in responsiveness is important in nonspecific inflammatory responses to irritant pollutants such as ozone and environmental tobacco smoke. These studies indicate that environmental factors influence primary allergen sensitization, secondary allergic responses, the activation of nonspecific inflammatory responses, and the severity of respiratory diseases, including asthma.
Assuntos
Poluição Ambiental/efeitos adversos , Hipersensibilidade Respiratória/epidemiologia , Adolescente , Adulto , Poluição do Ar em Ambientes Fechados/efeitos adversos , Alérgenos/efeitos adversos , América Central/epidemiologia , Criança , Humanos , América do Norte/epidemiologia , Razão de Chances , Prevalência , Hipersensibilidade Respiratória/etiologia , Testes Cutâneos , América do Sul/epidemiologiaRESUMO
We evaluated the effect of muscle paralysis on gas exchange and incidence of pneumothorax in 35 severely ill infants on mechanical ventilation. Pancuronium (0.1 mg/kg) was given repeatedly until spontaneous respirations ceased in infants with inadequate gas exchange with FIO2 greater than 0.60, or peak inspiratory pressure greater than 30 cm H2O, or who were breathing out of phase with the respirator. Of 27 infants who had an alveolar-arterial oxygen gradient greater than 300 torr before paralysis, AaDO2 improved by greater than 100 torr within one hour of paralysis in only two infants; it worsened in two infants within the same period. By six hours postparalysis, 12 of 27 infants had improved, five of whom had had a worsening AaDO2 before administration of pancuronium. Changes in oxygenation were unrelated to changes in arterial carbon dioxide tension in most infants. Peak transpulmonary pressures after paralysis were lower than during spontaneous breathing, and may explain the low incidence of pneumothorax (3 of 35) during paralysis. Since those who improved could not be distinguished by birth weight, gestational age, or diagnosis, pancuronium might be worthy of trial in a mechanically ventilated infant with severe lung disease who is at risk for pneumothorax.