shanek said:
NO ONE is making you smell anything! YOU take responsibility for YOUR actions, you hypocrite!
Bogus argument.
You turn the whole thing on its head.
If it was about individual responsibility, I'd never have breathed cigarette smoke indoors, outdoors, anywhere. I'd never have had to put up with this carcinogen.
MY arguments were about why the law was overdue in coming to protect the rights of non-smokers. Not about the legal standing of the legislation.
But you seem determined to draw me into an argument on that one.
All the laws in CA hinge on the hundreds of studies that show that Second-hand smoke causes illness.
And the fact that the laws in California have EVERY right to restrict what health hazards employers require of employees.
That's been court tested over and over again.
If you seriously want to argue that State Governments have no right to pass workplace health laws, that really cries out for another thread!
And I can send you info on dozens of studies on the effects of second-hand smoke. You deniers can take your shots, but WE know why you deny them all.
It's the freaky "Radar-Detector Libertarian" streak running in you. All about your rights (even your right to expose your workers to carcinogens), never about your responsibilities.
Here's a great study, that proves California's point exactly, about the health risks of people working in cigarette smoke:
"... Eisner et al.(1998) studied the association between ETS exposure and respiratory symptoms in a cohort of 53 bartenders before and after California's prohibition
on smoking in all bars and taverns. 74% of the bartenders initially reported respiratory symptoms; of those symptomatic at baseline, 59% no longer had symptoms at follow-up. 77% initially reported sensory irritation symptoms; at
follow-up, 78% of these had symptom resolution. "
Eisner MD, Smith AK, Blanc PD. Bartenders' respiratory health after establishment of smoke-free bars and taverns. JAMA 280:1909-1914 (1998).
From a summary of the studies at:
http://repace.com/fact_cardio.html
Here's some highlights, in small print, because it's just so many, and so overwhelming. But not to "Radar Detector Libertarians" who want to preserve their "right" to endanger the lives of others.
Law et al. (1997) review the evidence from 19 published studies of passive smoking and heart disease; they report that the average excess risk of ischemic heart disease from passive smoking epidemiological studies is 23% (95%
CI:14% to 33%), and conclude that platelet aggregation provides a plausible explanation for the mechanism and magnitude of the effect.
Kawachi, et al. (1997) in a prospective study of coronary heart disease (CHD) in 32,000 female U.S. nurses aged 31 to 61 yr., for nonsmoking women exposed only at work, observed a dose-response gradient for passive smoking and
CHD. Adjusted relative risks of CHD were 1.00 [for no exposure], 1.58 (95% CI, 0.93-2.68) [occasional exposure], and 1.91 (95% CI, 1.11-3.28) [regular exposure]. Thus, regular exposure to SHS at work caused a 91% increase in CHD.
1.No safe threshold has been established for cigarette smoking and risk of cardiovascular disease. Even smoking as few as 1-4 cigarettes per day is associated with a doubling in risk of coronary heart disease (CHD) ( Kawachi et
al., 1994).
2.Many cardiotoxic compounds are more concentrated in sidestream smoke than in mainstream smoke. For example, carbon monoxide (which is known to aggravate angina symptoms) is 8-11 times more concentrated in sidestream
smoke than mainstream smoke.(U.S. EPA, 1992)
3.At least seventeen epidemiological studies have been published on the relationship of passive smoking and risk of CHD. A meta-analysis of 19 studies (including three unpublished reports) found a summary relative risk of CHD
from exposure to spousal ETS of 1.30 (95% CI: 1.22 to 1.38, P < 0.001). (Law et al, 1997)
4.A meta-analysis of eight epidemiological studies of workplace ETS exposure and CHD found a summary relative risk of 1.18 (95% CI: 1.04 to 1.34).( Glantz and Parmley, 1991; 1995; Wells, 1998)
5.Several plausible mechanisms exist by which ETS exposure can increase the risk of CHD (Kawachi, 1998), including carboxyhemoglobinemia, increased platelet aggregability, increased fibrinogen levels, reduction in
HDL-cholesterol, and direct toxic effects of compounds such as 1,3 butadiene (a vapor phase constituent of ETS which has been shown to accelerate atherosclerosis in animal models (Penn and Snyder, 1996).
6.ETS exposure has also been linked to progression of atherosclerosis as measured by B-mode ultrasound of the carotid wall (Howard et al., 1994; Diez-Roux et al., 1995; Howard et al., 1998), as well as to early arterial damage as
assessed by endothelium-dependent brachial artery dilatation (Celermajer et al., 1996).
7.The death toll attributable to passive smoking from CHD is estimated to be 10 to 20 times as large as deaths from lung cancer (Wells, 1988, 1994; Glantz and Parmley, 1991; 1994; Steenland, 1992)
The most recent report on SHS from the UK, the SCOTH Report (1998), also concluded that passive smoking is a cause of lung cancer and childhood respiratory disease, and that passive smoking is a cause of ischaemic heart disease
and cot death (SIDS), middle ear disease and asthmatic attacks in children. The SCOTH report concludes that restrictions on smoking in public places and work places are necessary to protect non smokers (SCOTH, 1998).
