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Prenatal and early life periods represent critical windows for oxidant pollutant-induced lung remodeling. The objective of this study was to examine the association of prenatal and lifetime exposures to air pollutants with pulmonary function in a cohort of children with asthma.Prenatal and lifetime exposure to several air pollutants was reconstructed for 232 children with asthma from the San Joaquin Valley of California, USA. Prenatal and lifetime residences were geocoded. We obtained data on monthly average ozone (O3), carbon monoxide (CO), nitrogen dioxide (NO2), and particulate matter with a median aerodynamic diameter <10 μm (PM10) concentrations. Metrics were created for key developmental periods. Predictive models were developed for 8 pulmonary function measures. A newly-developed stepwise model selection procedure—the Deletion/Substitution/Addition algorithm—was implemented and results were compared with those obtained using traditional stepwise methods.Second-trimester exposure to NO2 negatively affected forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV1), and first trimester exposure to PM10 negatively affected peak expiratory flow (PEF) rate. Exposure to CO in early years of life also had a negative effect on FEV1/FVC and forced expiratory flow between 25% and 75% of FVC (FEF25-75)/FVC. Second trimester exposure to PM10 and exposure to CO in the first 6 years of life had negative effects on forced expiratory flow at 25% of FVC. Prenatal, but not trimester-specific, exposure to CO was negatively associated with FEF25-75. Effects were limited to subgroups, such as children who were African American, those diagnosed with asthma before the age of 2 years, and those exposed to maternal smoking during pregnancy.Prenatal and early-life exposures to CO, PM10, and NO2 have a negative effect on pulmonary function in subgroups of asthmatic children. [ABSTRACT FROM AUTHOR]

Background: Arsenic is a unique human carcinogen in that it causes lung cancer by exposure through ingestion (in drinking water) as well as through inhalation. Less is known about nonmalignant pulmonary disease after exposure to arsenic in drinking water.Methods: We recruited 108 subjects with arsenic-caused skin lesions and 150 subjects without lesions from a population survey of over 7000 people in an arsenic-exposed region in West Bengal, India. Thirty-eight study participants who reported at least 2 years of chronic cough underwent high-resolution computed tomography (CT); these scans were read by investigators in India and the United States without knowledge of the presence or absence of skin lesions.Results: The mean (+/-standard deviation) bronchiectasis severity score was 3.4 (+/-3.6) in the 27 participants with skin lesions and 0.9 (+/-1.6) in the 11 participants without these lesions. In subjects who reported chronic cough, CT evidence of bronchiectasis was found in 18 (67%) participants with skin lesions and 3 (27%) subjects without skin lesions. Overall, subjects with arsenic-caused skin lesions had a 10-fold increased prevalence of bronchiectasis compared with subjects who did not have skin lesions (adjusted odds ratio=10; 95% confidence interval=2.7-37).Conclusions: These results suggest that, in addition to being a cause of lung cancer, ingestion of high concentrations of arsenic in drinking water may be a cause of bronchiectasis. [ABSTRACT FROM AUTHOR]

Background: Tropospheric ozone (O3) is an oxidant, outdoor air pollutant. Chronic exposure has been associated with decreased lung function in children and adolescents. This study investigated the effects of long-term exposure to O3 on lung function in college freshmen.Methods: We recruited University of California, Berkeley students (n=255) who were lifelong residents of the Los Angeles and San Francisco Bay areas and who never smoked. Lifetime exposures to O3, small particulate matter (PM10), and nitrogen dioxide (NO2) were based on spatial interpolation of compliance monitor measurements to all residences at which students lived. Spirometry was performed between February and May, times when students would not have had recent exposure to increased levels of O3.Results: Lifetime exposure to O3 was associated with decreased levels of measures of small airways (<2 mm) function (FEF75 and FEF25-75). There was an interaction with the FEF25-75/FVC ratio, a measure of intrinsic airway size. Subjects with a large ratio were less likely to have decreases in FEF75 and FEF25-75 for a given estimated lifetime exposure to O3. This association was not altered by history of chronic respiratory disease, allergy, second-hand exposure to environmental tobacco smoke, exposure to PM10 and NO2, or measurement errors in exposure assessment.Conclusions: A history of increased level of lifetime exposure to ambient O3 is associated with decreased function of airways in which O3 deposition in the lungs is the greatest. Adolescents with intrinsically smaller airways appear to be at greatest risk. Any environmental or genetic factors that lead to reduced airway size may lead to increased susceptibility to the adverse effects of ambient ozone. [ABSTRACT FROM AUTHOR]