The Calif. Air Resources Board (CARB) finalized its ban on ozone generators for occupied spaces on Sept. 18, 2008. The ban takes effect in Fall 2010. It does not affect units that only filter the air. CARB was required to adopt the regulations by 12-31-08 pursuant to Assembly Bill 2276 enacted in 2006.
For more info, see www.arb.ca.gov/regact/2007/iacd07/iacd07.htm.
Archive for the ‘Air Pollutants’ Category
The Calif. Air Resources Board (CARB) finalized its ban on ozone generators
Monday, February 9th, 2009Indoor volatile organic compounds: concentrations, sources, variation factors
Monday, February 9th, 2009Rev Mal Respir. 2008 Jun;25(6):725-30.
[Indoor volatile organic compounds: concentrations, sources, variation factors.]
[Article in French]
Palot A, Charpin-Kadouch C, Ercoli J, Charpin D.
Service de pneumologie-allergologie, Hôpital Nord, Marseille et EA1784 IFR 112, Université de la Méditerranée, France.
Introduction Volatile organic compounds (V.O.C.) are part of urban air pollution and are also generated indoors from cleaning and maintenance products. Background VOC measurements are, on average, 10 times higher within homes than outside. Results of the national survey led by the Observatoire National de la Qualité de l’Air Intérieur demonstrated that up to 25% of French homes have very high or high concentrations of VOC. Indoor levels depend mainly on indoor sources. Aldehydes are included in many everyday life products. VOC originate from various household decorating and cleaning products. Some products are less detrimental to the environment and health and have special labelling. Indoor VOC levels also depend on the rate of air exchange and on household characteristics such as indoor temperature and humidity, age of the building, presence of smokers, and communication with a garage. Viewpoints The public may participate in maintaining good indoor air quality and the authorities should also improve regulations. Conclusion VOC are part of everyday air pollution. Their sources and concentrations should be better monitored.
PMID: 18772829 [PubMed - in process]
http://www.ncbi.nlm.nih.gov/pubmed/18772829?dopt=AbstractPlus
Health Effects of Subchronic Inhalation Exposure to Gasoline Engine Exhaust.
Friday, February 6th, 2009Inhal 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]
Indoor Air Quality report of the National Institute for Building Resear
Friday, February 6th, 2009Several builders and remodelers have approached me about serving the needs of the chemically sensitive during this time of reduced building activity. They are ecstatic about the Indoor Air Quality report of the National Institute for Building Research. Several of us who work with chemically sensitive people got the U.S. Access Board to fund this report.
In this regard, we are especially indebted to Mary Lamielle, Susan Molloy, Dr. Ann McCampbell, and Toni Temple. The Access Board sets the standards for accommodation of people with disabilities. Builders are particularly interested in the sections starting on p. 86 dealing with building products.
http://ieq.nibs.org/ieq_project.pdf
I recommend that you tell builders interested in green building in your area about this report.
Lawrence Plumlee, M.D.
Systemic inflammation, endothelial dysfunction, and activation in clinically healthy children exposed to air pollutants.
Wednesday, January 28th, 2009Inhal 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]
