Canvassing for Opinion - aka "Blairs Brain on Cannabis"

IMHO prohibition sentiment requires inherent addiction to status quo, an incapacity to visualise beyond the here and now and a desperate desire to know others might feel the same... Reform is not revolutionary, rather it is evolutionary. Having survived banging your head against a brick wall the evolutionist relishes having stopped. / Blair

Friday, February 02, 2007

PM2.5 is a risk whether ya sit or stand, bike or hike.

Results A total of 1816 women had one or more fatal or nonfatal cardiovascular events, as confirmed by a review of medical records, including death from coronary heart disease or cerebrovascular disease, coronary revascularization, myocardial infarction, and stroke. In 2000, levels of PM2.5 exposure varied from 3.4 to 28.3 µg per cubic meter (mean, 13.5). Each increase of 10 µg per cubic meter was associated with a 24% increase in the risk of a cardiovascular event (hazard ratio, 1.24; 95% confidence interval [CI], 1.09 to 1.41) and a 76% increase in the risk of death from cardiovascular disease [Dockery/Stone N Engl J Med 2007 Feb 1; 356:511-3.]
Oooww... Another Blair was 'dead' right again moment (grin)
My Notes: In this excellent new public health research the levels of cumulative exposure [behaviour mediated] are not being measured. However even the ambient PM2.5 exposure had a mean, one quarter of current accepted 'do not exceed over 24hrs' limits and the maximum range studied [ 28.3µg/m3] is just about one half of the 50µgm3 / 24hrs 'artificial red line' used as OUR margin of safety, by ECAN.
Our present strategy is to not exceed 50µg/m3 more than ten times/pa.. The rule in effect fills up the cumulative exposure until we have no more room.. ie 49.99µg/m3 is OK public policy. 2/100ths more is not.
That this research is way within the exposure guideline parameters makes is especially interesting as it points to health and safety gains especially for those who work and live in high exposure occupations and recreations; and identifies moreso for woman over 50yrs, to mediate that risk. The greatest and immediate 'low cost' intervention is behavioural, in mediating exposure. (ie not cycling in heavy traffic; PM cumulative exposure is correlated proportionally to oxygen uptake!). All this is not withstanding what emitters can do, ie: biofuels/biodiesel, and urban planners cf: city mall redevelopment)
[Some jurisdictions have recently reduced the PM permitted levels from 50µg/m3 down to 30µg/m3 as a precautionary measure ]
Also, their is the negative consequence of exercise avoidance [ie public transport/private motor] that exacerbates cardiovascular risk via the obesity etiology.
The earlier studies suggested the elevated risk overall rose 7% per 10µg, this more robust study suggests with confidence a 24% increase; I am not surprised.
It is far more realistic to correlate PM2.5 than PM10 to health outcomes. PM2.5 is about 90% [by weight] of the PM10 emission which in US cities as it is in Christchurch PM2.5 comes primarily from mobile source arterial traffic volumes, mostly diesel. These particulates are Poly Aromatic Hydrocarbons (benzene rings) aggregating on activated carbon with heavy metals. [They are also carcinogenic/terragenic. ]
A useful measure 'of public heath risk' in this case is the speed made good by these emitting classes of vehicle [I analysed this back in 2001 using latest software that spatially models PM emissions]. see http://mildgreens.com/biosafe/efactor.jpg
These emission's have recently been measured in the elevated poor health outcomes of children who live close to arterial/motorways (500m) compared to those who live 1500m away. The prognosis for a significant number is chronic.
Someone suffering a pollution-related deficit in lung function as a child will probably have less than healthy lungs all of his or her life," said lead author W. James Gauderman, associate professor of preventive medicine at the Keck School of Medicine. " And poor lung function in later adult life is known to be a major risk factor for respiratory and cardiovascular diseases."

The report draws upon data from the Children's Health Study, a longitudinal document of respiratory health among children in 12 Southern California communities. More than 3,600 children around the age of 10 were evaluated over a period of eight years, through high school graduation. Lung function tests were taken during annual school visits, and the study team determined how far each child lived from freeways and other major roads.

"Otherwise-healthy children who were non-asthmatic and non-smokers also experienced a significant decrease in lung function from traffic pollution," Gauderman said. "This suggests that all children, not just susceptible subgroups, are potentially affected by traffic exposure."

Lung function was assessed by measuring how much air a person can exhale after taking a deep breath and how quickly that air can be exhaled. Children's lung function develops rapidly during adolescence until they reach their late teens or early 20s. A deficit in lung development during childhood is likely to translate into reduced function for the remainder of life.

"This study shows there are health effects from childhood exposure to traffic exhaust that can last a lifetime," said David A. Schwartz, director of the National Institute of Environmental Health Sciences. "The [institute] is committed to supporting research to understand the relationship between environmental exposures and diseases, and to identify ways to reduce harmful exposures to all populations, especially children so they can realize their full potential for healthy and productive lives."

Previous studies have demonstrated links between lung function growth and regional air quality. The findings in this study add to that result, demonstrating that both regional air pollution and local exposure to traffic pollution affect lung development .

"This study provides further proof that regional air quality regulations may need to be adjusted based on local factors, including traffic volume," Gauderman said. "This is important because in areas where the population continues to grow, more and more children are living or attending school near busy roadways. This may be harmful in the long run."

Gauderman added that community leaders, school districts and developers should consider these results when developing new schools or homes.
None of this is surprising. From this 'ambient air' data set I get a very close 'fit' to my CHCH forecast (70 additional deaths/pa ) but any variation would likely be accounted as I was not gender, or in this NEJM paper, age specific. For Christchurch, the "air shed" risk over a lifetime is about 4 times that of contributing to the road toll.
Again it is about public education about cumulative exposure - ie: exercise in the morning, not during peak hour traffic and away from congested arterial. blah blah. 'while we fix the air, at least'
(I could kick Garry Moore in the arteries over this one! - And if they were standing nearby, Prof. Ian Townes and Evon Currie (CDHB) too as it was they AND the mayor who oversaw my being dismissed to 'unhealthy Christchurch'. )
PM2.5 is a risk whether ya sit or stand, bike or hike, Mal [ Briesman ].
(Now wouldn't it be funny if I was to read in Cardiology Watch :Cannabinoids Retard Progression of Atherosclerosis)
/ Blair

Air Pollution and Cardiovascular Risk

Exposure differences within cities matter, according to Women's Health Initiative data.

The Women's Health Initiative Observational Study, a study of postmenopausal women age 50 to 79, gave investigators an opportunity to elucidate the effect of air pollution on the risk for cardiovascular disease (CVD). The current analysis included the 65,893 subjects who were free of CVD at baseline, returned a follow-up questionnaire annually, and could be matched by residence area to a nearby measurement of particulate matter (obtained by the Environmental Protection Agency).

During follow-up (median, 6 years), 1816 subjects had a first cardiovascular event (MI, revascularization, stroke, or death from either coronary heart disease or cerebrovascular disease). Each 10-µg/m3 increase in the level of PM2.5 (particulate matter <2.5 µm in diameter) was associated with significantly increased risks for cardiovascular events (adjusted hazard ratio, 1.24) and death definitely linked to coronary heart disease (AHR, 2.21). Air pollution also was associated with increased risks for stroke and death from stroke.

Comment: This study substantially strengthens the evidence linking air pollution and CVD (e.g.,Journal Watch Cardiology Jan 7 2005 ). Prior studies have focused on differences between cities, whereas this study, which found substantial within-city variation, shows a strong association at the level of the individual. The mechanisms by which fine particulate matter may mediate vascular risk are yet to be understood, but these findings suggest that efforts to control air pollution might reduce cardiovascular risk.

— Harlan M. Krumholz, MD, SM

Published in Journal Watch Cardiology January 31, 2007

Citation(s):

Miller KA et al. Long-term exposure to air pollution and incidence of cardiovascular events in women. N Engl J Med 2007 Feb 1; 356:447-58.
[Original article]

Dockery DW and Stone PH. Cardiovascular risks from fine particulate air pollution. N Engl J Med 2007 Feb 1; 356:511-3.
[Original article]

--
/Blair Anderson
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