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Is there an association between lifetime cumulative exposure and acute pulmonary responses to ozone?

ABSTRACT: To investigate the potential effects of lifetime cumulative ozone (O3) exposure on acute pulmonary responses to O3.Fifteen healthy subjects from a larger cohort of young adults were exposed to 200 ppb O3 for 4 hours followed by bronchoscopy and bronchoalveolar lavage 18 hours later. Lung function, symptom questionnaires, and blood samples were obtained before and after each exposure. Subjects' lifetime cumulative O3 exposures were estimated from residential histories and air-quality monitoring data.Acute exposure to O3 caused decrements in forced expiratory volume in 1 second (FEV1), maximal mid-expiratory flow rate (FEF25-75), and forced expiratory flow rate at 75% of forced vital capacity (FEF75), and an increase in plasma clara cell protein (CC16) level. Changes in CC16 and lower respiratory symptoms, but not in lung function, were positively correlated with lifetime cumulative O3 exposure.Higher lifetime cumulative O3 exposure was associated with airway injury and respiratory symptom responses, but not with airway inflammatory or lung function responses, to acute O3 exposure.

SUBMITTER: Arjomandi M

PROVIDER: S-EPMC3321313 | biostudies-literature | 2008 Mar

REPOSITORIES: biostudies-literature

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Is there an association between lifetime cumulative exposure and acute pulmonary responses to ozone?

Arjomandi Mehrdad M Tager Ira B IB Bastaki Maria M Chen Connie C Holland Nina N Balmes John R JR

Journal of occupational and environmental medicine 20080301 3

<h4>Objective</h4>To investigate the potential effects of lifetime cumulative ozone (O3) exposure on acute pulmonary responses to O3.<h4>Methods</h4>Fifteen healthy subjects from a larger cohort of young adults were exposed to 200 ppb O3 for 4 hours followed by bronchoscopy and bronchoalveolar lavage 18 hours later. Lung function, symptom questionnaires, and blood samples were obtained before and after each exposure. Subjects' lifetime cumulative O3 exposures were estimated from residential hist ...[more]

PMID: 18332784

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Project description:BackgroundExposure to environmental toxicants may play a role in the pathogenesis of Non Alcoholic Fatty Liver Disease (NAFLD). Cumulative exposure to lead (Pb) has chronic and permanent effects on liver function. Pediatric populations are vulnerable to the toxic effects of Pb, even at low exposure levels. The purpose of the study was to estimate the association between cumulative Pb exposure during childhood and hepatic steatosis biomarkers in young Mexican adults.MethodsA subsample of 93 participants from the ELEMENT cohort were included in this study. Childhood blood samples were collected annually from ages 1-4 years and were used to calculate the Cumulative Childhood Blood Lead Levels (CCBLL). Hepatic steatosis during adulthood was defined as an excessive accumulation of hepatic triglycerides (>5%) determined using Magnetic Resonance Imaging (MRI). Liver enzymes were also measured at this time, and elevated liver enzyme levels were defined as ALT (≥30 IU/L), AST (≥30 IU/L), and GGT (≥40 IU/L). Adjusted linear regression models were fit to examine the association between CCBLL (quartiles) and the hepatic steatosis in young adulthood.ResultsIn adulthood, the mean age was 21.4 years, 55% were male. The overall prevalence of hepatic steatosis by MRI was 19%. Elevate levels of the enzymes ALT, AST, and GGT were present in 25%, 15%, and 17% of the sample, respectively. We found a positive association between the highest quartile of CCBLL with the steatosis biomarkers of hepatic triglycerides (Q4 vs. Q1: β = 6.07, 95% CI: 1.91-10.21), elevated ALT (Q4 vs. Q1: β = 14.5, 95% CI: 1.39-27.61) and elevated AST (Q4 vs. Q1: β = 7.23, 95% CI: 0.64-13.82). No significant associations were found with GGT.ConclusionsChronic Pb exposure during early childhood is associated with a higher levels of hepatic steatosis biomarkers and hepatocellular injury in young adulthood. More actions should be taken to eliminate sources of Pb during the first years of life.

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Is there an association between lifetime cumulative exposure and acute pulmonary responses to ozone?

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Is there an association between lifetime cumulative exposure and acute pulmonary responses to ozone?

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