Posts Tagged ‘Inhal Toxicol’

Low level of exposure to pesticides leads to lung dysfunction in occupationally exposed subjects.

Tuesday, February 10th, 2009

Inhal Toxicol. 2008 Jul;20(9):839-49. Links

Low level of exposure to pesticides leads to lung dysfunction in occupationally exposed subjects.
Hernández AF, Casado I, Pena G, Gil F, Villanueva E, Pla A.

Department of Legal Medicine and Toxicology, University of Granada Medical School, Granada, Spain. ajerez@ugr.es

Pesticides may contribute to adverse respiratory health effects among farmers and have been considered one causal factor for the rise in asthma prevalence. This cross-sectional study was conducted to evaluate potential respiratory function abnormalities following long-term pesticide exposure by means of a complete pulmonary function testing, including spirometry, lung volumes, and diffusing capacity for carbon monoxide. The study population was comprised by workers from a prominent intensive agriculture area of southern Spain that relied on pesticides for the control of plagues. Eighty-nine pesticide sprayers of plastic greenhouse farming and a control group of 25 nonspraying control farmers from the same area were interviewed by a general practitioner asking about sociodemographic factors, occupational exposure, and clinical symptoms by using a structured questionnaire. Multiple regression analyses showed a relationship of short-term exposure to pesticides (as indicated by a drop in serum cholinesterase > 25% of baseline levels) with reduced forced expired volume in 1 s, and of long-term exposure (as indicated by a cumulative pesticide exposure index) with reduced forced expiratory flow rate. Exposure to bipyridilium-class herbicides was a determinant of a fall in the diffusing capacity of the lungs, and neonicotinoid insecticides showed a relationship with lower pulmonary volumes (total lung capacity, residual volume, and functional residual capacity), suggestive of restrictive lung disease, and with an increased risk of reporting irritative symptoms.

PMID: 18645724 [PubMed - indexed for MEDLINE] Inhal Toxicol. 2008 Jul;20(9):839-49. Links

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Posted in Environmental Toxicants, Pesticides | No Comments »

Health Effects of Subchronic Inhalation Exposure to Gasoline Engine Exhaust.

Friday, February 6th, 2009

Inhal Toxicol. 2008 Sep 18:1. [Epub ahead of print]

Health Effects of Subchronic Inhalation Exposure to Gasoline Engine Exhaust.
Reed MD, Barrett EG, Campen MJ, Divine KK, Gigliotti AP, McDonald JD, Seagrave JC, Mauderly JL, Seilkop SK, Swenberg JA.

Lovelace Respiratory Research Institute, Albuquerque, NewMexico, USA.
Gasoline engine emissions are a ubiquitous source of exposure to complex mixtures of particulate matter (PM) and non-PM pollutants; yet their health hazards have received little study in comparison with those of diesel emissions. As a component of the National Environmental Respiratory Center (NERC) multipollutant research program, F344 and SHR rats and A/J, C57BL/6, and BALBc mice were exposed 6 h/day, 7 days/week for 1 week to 6 months to exhaust from 1996 General Motors 4.3-L engines burning national average fuel on a simulated urban operating cycle. Exposure groups included whole exhaust diluted 1:10, 1:15, or 1:90, filtered exhaust at the 1:10 dilution, or clean air controls. Evaluations included organ weight, histopathology, hematology, serum chemistry, bronchoalveolar lavage, cardiac electrophysiology, micronuclei in circulating cells, DNA methylation and oxidative injury, clearance of Pseudomonas aeruginosa from the lung, and development of respiratory allergic responses to ovalbumin. Among the 120 outcome variables, only 20 demonstrated significant exposure effects. Several statistically significant effects appeared isolated and were not supported by related variables. The most coherent and consistent effects were those related to increased red blood cells, interpreted as likely to have resulted from exposure to 13-107 ppm carbon monoxide. Other effects supported by multiple variables included mild lung irritation and depression of oxidant production by alveolar macrophages. The lowest exposure level caused no significant effects. Because only 6 of the 20 significant effects appeared to be substantially reversed by PM filtration, the majority of effects were apparently caused by non-PM components of exhaust.

http://www.ncbi.nlm.nih.gov/pubmed/18800271?dopt=AbstractPlus

PMID: 18800271 [PubMed - as supplied by publisher]

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Posted in Air Pollutants | No Comments »

Systemic inflammation, endothelial dysfunction, and activation in clinically healthy children exposed to air pollutants.

Wednesday, January 28th, 2009

Inhal Toxicol. 2008 Mar;20(5):499-506.

Systemic inflammation, endothelial dysfunction, and activation in clinically healthy children exposed to air pollutants.
Calderón-Garcidueñas L, Villarreal-Calderon R, Valencia-Salazar G, Henríquez-Roldán C, Gutiérrez-Castrellón P, Torres-Jardón R, Osnaya-Brizuela N, Romero L, Torres-Jardón R, Solt A, Reed W.

Instituto Nacional de Pediatría, Mexico City, Mexico.

Mexico City children are chronically exposed to significant concentrations of air pollutants and exhibit chronic respiratory-tract inflammation. Epidemiological, controlled human exposures, laboratory-based animal models, and in vitro/in vivo studies have shown that inflammatory, endothelial dysfunction, and endothelial damage mediators are upregulated upon exposure to particulate matter (PM). Endothelial dysfunction is a critical event in cardiovascular disease. The focus of this work was to investigate whether exposure to ambient air pollution including PM(2.5) produces systemic inflammation and endothelial injury in healthy children. We measured markers of endothelial activation, and inflammatory mediators in 52 children age 8.6+/-0.1 yr, residents of Mexico City (n: 28) or of Polotitlán (n: 24), a city with low levels of pollutants. Mexico City children had significant increases in inflammatory mediators and vasoconstrictors, including tumor necrosis factor (TNF)alpha, prostaglandin (PG) E2, C-reactive protein, interleukin-1beta, and endothelin-1. There was a significant anti-inflammatory response, and a downregulation of vascular adhesion molecule-1, intercellular adhesion molecule-1 and -2, and selectins sE and sL. Results from linear regression found TNF a positively associated with 24- and 48-h cumulative levels of PM(2.5), while the 7-d PM(2.5) value was negatively associated with the numbers of white blood cells in peripheral blood in highly exposed children. Systemic subclinical inflammation, increased endothelin- 1, and significant downregulation of soluble adhesion molecules are seen in Mexico City children. Children chronically exposed to fine PM above the standard could be at risk of developing cardiovascular diseases, atherosclerosis, stroke, and other systemic effects later in life.

PMID: 18368620 [PubMed - in process]

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Posted in Air Pollutants, Children | No Comments »