nitrogen-dioxide and Lead-Poisoning

Over the past three or four decades, there have been important advances in the understanding of the actions, exposure-response characteristics, and mechanisms of action of many common air pollutants. A multidisciplinary approach using epidemiology, animal toxicology, and controlled human exposure studies has contributed to the database. This review will emphasize studies of humans but will also draw on findings from the other disciplines. Air pollutants have been shown to cause responses ranging from reversible changes in respiratory symptoms and lung function, changes in airway reactivity and inflammation, structural remodeling of pulmonary airways, and impairment of pulmonary host defenses, to increased respiratory morbidity and mortality. Quantitative and qualitative understanding of the effects of a small group of air pollutants has advanced considerably, but the understanding is by no means complete, and the breadth of effects of all air pollutants is only partially understood.

Topics: Acids; Air Pollutants; Carbon Monoxide; Humans; Lead Poisoning; Nitrogen Dioxide; Ozone; Sulfur Dioxide

Topics: Aerosols; Air Pollution; Animals; Asbestos; Benzopyrenes; Cricetinae; Dust; Gases; Guinea Pigs; Humans; Hypersensitivity; Injections, Subcutaneous; Iron; Lead; Lead Poisoning; Lung Neoplasms; Mice; Nitrogen Dioxide; Ozone; Rats; Research Design; Skin Absorption; Smoking; Sulfur Dioxide; Time Factors; Vehicle Emissions

Topics: Aerosols; Air Pollution; Aldehydes; Asthma; Atmosphere; Beryllium; Bronchitis; Carbon Monoxide Poisoning; Carcinogens; Environmental Health; Europe; Formaldehyde; Gases; Humans; Hydrocarbons; Japan; Lead Poisoning; Nitrogen; Nitrogen Dioxide; Ozone; Petroleum; Pulmonary Emphysema; Respiratory Tract Diseases; Sulfur; Sulfur Dioxide; Sulfuric Acids; Toxicology; United States

Topics: Air Pollutants; Air Pollution; Beryllium; Carbon Monoxide Poisoning; Carcinogens; Fluorides; Humans; Lead Poisoning; Nitrogen; Nitrogen Dioxide; Ozone; Sulfides; Sulfur; Sulfur Dioxide; Toxicology

Lead-based paint remains a pervasive problem in U.S. cities, and an increasing problem in the developing world where it is still manufactured and used. Little attention has focused on the factors that increase the release of lead pigment granules from painted surfaces. Nitrogen dioxide (NO(2)) and ozone (O(3)) from transportation emissions in urban environments have the potential to react with and remove polymeric binders in paint, making pigment granules more available for subsequent transfer to hands on contact, or deposition in housedust. Here we show that exposure to NO(2) and O(3) increased the lead in wipe samples of stainless steel surfaces painted with alkyd low gloss solvent lead-based paint by 296% +/- 101 (or 0.24 microg/cm(2)) and 37% +/- 21 (or 0.025 microg/cm(2)), respectively, with corresponding changes in surface morphology indicated by reflectometry and scanning electron microscopy. Lead release from unexposed low gloss acrylic household paints was 40 times greater than comparable solvent based paints. Given that lead-based paint is still manufactured and used in many urban areas of the developing world where O(3) concentrations currently exceed historic U.S. concentrations, the interaction of air pollution with lead painted indoor surfaces may pose greater exposure risks for lead poisoning in children than previously anticipated.

Topics: Environmental Pollutants; Humans; Lead; Lead Poisoning; Nitrogen Dioxide; Ozone; Paint

We have recently found evidence for increased reactive oxygen species (ROS) in rats with lead-induced hypertension. We hypothesized that increased ROS activity may contribute to hypertension by enhancing inactivation of nitric oxide (NO) in this model.. Rats were treated for 12 weeks with either lead acetate (100 p.p.m.) alone (Pb group) or lead acetate plus vitamin E-fortified food (5000 U/kg rat chow, Pb + E group). The control animals were fed either regular rat chow or a vitamin E-fortified diet. Blood pressure, creatinine clearance, and urinary excretion of stable NO metabolites (NOx) were monitored, and plasma and tissue abundance of nitrotyrosine, which is the footprint of NO oxidation by ROS, were determined.. The Pb group showed a marked rise in blood pressure, a significant increase in plasma and kidney, heart, liver, and brain nitrotyrosine abundance, and a substantial fall in urinary NOx excretion. Concomitant administration of high-dose vitamin E in the Pb + E group ameliorated hypertension and normalized both urinary NOx excretion and tissue nitrotyrosine without altering tissue lead content. However, vitamin E supplementation had no discernible effect on either blood pressure or nitrotyrosine abundance in the normal controls.. These findings point to enhanced ROS-mediated inactivation and sequestration of NO, which can potentially contribute to hypertension, tissue damage, and reduced urinary NOx excretion in rats with lead-induced hypertension. The beneficial effects of high-dose vitamin E on blood pressure, tissue nitrotyrosine burden, and urinary NOx excretion support the role of increased ROS activity in the pathogenesis of these abnormalities in this model.

Topics: Animals; Antioxidants; Blood Pressure; Blotting, Western; Brain Chemistry; Hypertension, Renal; Kidney; Lead; Lead Poisoning; Liver; Male; Myocardium; Nitric Oxide; Nitrogen Dioxide; Oxidation-Reduction; Rats; Rats, Sprague-Dawley; Reactive Oxygen Species; Tyrosine; Vitamin E

Topics: Air Pollution; Animals; Bromides; Carbon Monoxide Poisoning; Chlorides; Erythrocytes; Female; Haplorhini; Kidney; Lead; Lead Poisoning; Levulinic Acids; Macaca; Male; Nitrogen Dioxide; Osmotic Fragility; Porphyrins; Rats; Sulfur Dioxide