Temporal and spatial patterns of ambient endotoxin concentrations in Fresno, California.

BACKGROUND: Endotoxins are found in indoor dust generated by human activity and pets, in soil, and adsorbed onto the surfaces of ambient combustion particles. Endotoxin concentrations have been associated with respiratory symptoms and the risk of atopy and asthma in children. OBJECTIVE: We characterized the temporal and spatial variability of ambient endotoxin in Fresno/Clovis, California, located in California's Central Valley, to identify correlates and potential predictors of ambient endotoxin concentrations in a cohort of children with asthma [Fresno Asthmatic Children's Environment Study (FACES)]. METHODS: Between May 2001 and October 2004, daily ambient endotoxin and air pollutants were collected at the central ambient monitoring site of the California Air Resources Board in Fresno and, for shorter time periods, at 10 schools and indoors and outdoors at 84 residences in the community. Analyses were restricted to May-October, the dry months during which endotoxin concentrations are highest. RESULTS: Daily endotoxin concentration patterns were determined mainly by meteorologic factors, particularly the degree of air stagnation. Overall concentrations were lowest in areas distant from agricultural activities. Highest concentrations were found in areas immediately downwind from agricultural/pasture land. Among three other measured air pollutants [fine particulate matter, elemental carbon (a marker of traffic in Fresno), and coarse particulate matter (PMc)], PMc was the only pollutant correlated with endotoxin. Endotoxin, however, was the most spatially variable. CONCLUSIONS: Our data support the need to evaluate the spatial/temporal variability of endotoxin concentrations, rather than relying on a few measurements made at one location, in studies of exposure and and respiratory health effects, particularly in children with asthma and other chronic respiratory diseases.

Early-lifetime exposure to air pollution and allergic sensitization in children with asthma.

Observations on the association between exposure to common outdoor air pollutants and allergic sensitization have not been consistent. Little research has been done on the effects of prenatal exposure or the effect among asthmatics. The association between prenatal and early-life exposures and outdoor air pollutants with allergic sensitization was examined within a cohort of 170 children ages 6-11 years with asthma, living in the Central Valley of California. Allergic sensitization was ascertained by skin-prick tests to 14 allergens. Prenatal and early-life exposure to ozone (O(3)), nitrogen dioxide (NO(2)), carbon monoxide (CO) and particulate matter with a median aerodynamic diameter < 10 micro m (PM(10)) was reconstructed for each child. Models were developed for sensitized to (a) any allergen, (b) at least one outdoor allergen, and (c) at least one indoor allergen. In multivariable analyses, higher exposure to CO during pregnancy was associated with an increased risk of sensitization to at least one outdoor allergen. The largest effect was seen for the association between exposure to 8-hour daily maximum CO during pregnancy and sensitization to at least one outdoor allergen. (OR = 1.55 (95% CI: 1.01, 2.37)) per interquartile range (IQR) increase.) Similar effects estimates were seen for 2nd trimester exposure to CO, but these were less precisely estimated (OR = 1.45 (95%CI: 0.90, 2.35)). No significant associations with the pollutants were seen for sensitization to allergens in general or to at least one indoor allergen. Exposure to traffic-related pollutants during pregnancy may increase the risk of sensitization to outdoor allergens among asthmatic children.

Air pollution and pulmonary function in asthmatic children: effects of prenatal and lifetime exposures.

BACKGROUND: 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. METHODS: 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 microm (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. RESULTS: 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. CONCLUSION: Prenatal and early-life exposures to CO, PM10, and NO2 have a negative effect on pulmonary function in subgroups of asthmatic children.

Chronic exposure to ambient ozone and lung function in young adults.

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.