Workers' compensation systems attempt to evaluate claims for occupational disease on an individual basis using the best guidelines available to them. This may be difficult when there is more than one risk factor associated with the outcome, such as asbestos and cigarette smoking, and the occupational exposures is not clearly responsible for the disease. Apportionment is an approach that involves an assessment of the relative contribution of work-related exposures to the risk of the disease or to the final impairment that arises for the disease. This article discusses the concept of apportionment and applies it to asbestos-associated disease. Lung cancer is not subject to a simple tradeoff between asbestos exposure and smoking because of the powerful biological interaction between the two exposures. Among nonsmokers, lung cancer is sufficiently rare that an association with asbestos can be assumed if exposure has occurred. Available data suggest that asbestos exposure almost invariably contributes to risk among smokers to the extent that a relationship to work can be presumed. Thus, comparisons of magnitude of risk between smokers and nonsmokers are irrelevant for this purpose. Indicators of sufficient exposure to cause lung cancer are useful for purposes of establishing eligibility and screening claims. These may include a chest film classified by the ILO system as 1/0 or greater (although 0/1 does not rule out an association) or a history of exposure roughly equal to or greater than 40 fibres/cm3 x y. (In Germany, 25 fibres/cm3 x y is used.) The mere presence of pleural plaques is not sufficient. Mesothelioma is almost always associated with asbestos exposure and the association should be considered presumed until proven otherwise in the individual case. These are situations in which only risk of a disease is apportioned because the impairment would be the same given the disease whatever the cause. Asbestosis, if the diagnosis is correct, is by definition an occupational disease unless there is some source of massive environmental exposure; it is always presumed to be work-related unless proven otherwise. Chronic obstructive airways disease (COAD) accompanies asbestosis but may also occur in the context of minimal parenchymal fibrosis and may contribute to accelerated loss of pulmonary function. In some patients, particularly those with smoking-induced emphysema, this may contribute significantly to functional impairment. An exposure history of 10 fibre x years is suggested as the minimum associated with a demonstrable effect on impairment, given available data. Equity issues associated with apportionment include the different criteria that must be applied to different disorders for apportionment to work, the management of future risk (eg. risk of lung cancer for those who have asbestosis), and the narrow range in which apportionment is really useful in asbestos-associated disorders. Apportionment, attractive as it may be as an approach to the adjudication of asbestos-related disease, is difficult to apply in practice. Even so, these models may serve as a general guide to the assessment of asbestos-related disease outcomes for purposes of compensation.
The impact of four effective population-based interventions, focusing on individual behavioural change and aimed at reducing tobacco-attributable morbidity, was assessed by modeling with respect to effects on reducing prevalence rates of cigarette smoking, population-attributable fractions, reductions of disease-specific morbidity and its cost for Canada. Results revealed that an implementation of a combination of four tobacco policy interventions would result in a savings of 33,307 acute care hospital days, which translates to a cost savings of about $37 million per year in Canada. Assuming 40% coverage rate for all individually based interventions, the two most effective interventions, in terms of avoidable burden due to morbidity, would be nicotine replacement therapy and physicians' advice, followed by individual behavioural counselling and increasing taxes by 10%. Although a sizable reduction in the number of hospital days and accumulated costs could be achieved, overall these interventions would reduce less than 3% of all tobacco-attributable costs in Canada.
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Smoking is the leading preventable cause of premature death and disability in Canadian women. Lung cancer, ischemic heart disease, chronic obstructive lung disease, and stroke account for two-thirds or more of the smoking-attributable deaths in women. Lung cancer now exceeds breast cancer as the leading cause of cancer death in women, and both incidence and mortality rates continue to climb. Strong evidence suggests that for the same number of cigarettes smoked, women are more susceptible than men to the carcinogenic effects on their lungs. Evidence also is growing that lung function in women is more adversely affected by smoking and that smoking may be a stronger risk factor for myocardial infarction in women than it is in men. More research into the mechanisms underlying these gender-related susceptibilities is needed. Policies and programs to prevent girls from starting to smoke and to facilitate quitting in women of all ages must be public health priorities.
Smoking and obesity are two of the most important risk factors for chronic disease today. Their combined effect on the risk of disability pension is not known.
A nationwide cohort of 45 920 Swedish men (18.7 + or - 0.5 years) were followed for 38 years. The body mass index (BMI), based on measured height and weight, was used to define underweight ( or = 30.0). The hazard ratios (HRs) associated with BMI and smoking status at baseline for receiving disability pension were adjusted for socio-economic index (SEI), muscular strength, geographic region and place of residence.
During 1.6 million person-years, 4631 disability pensions and 2897 deaths occurred. After adjustment, overweight (HR 1.34, 95% CI 1.19-1.51) and obesity (HR 1.55, 1.18-2.05) were associated with an increased risk of disability pension, independent of smoking, whereas underweight (18.5; HR 1.07, 0.97-1.17) was not compared with normal weight. Similarly, smoking 1-10 (HR 1.37, 1.27-1.49) or >10 cigarettes per day (HR 2.01, 1.86-2.17) showed independent risk increases versus non-smoking. Although obese individuals smoking >10 daily cigarettes were at greatly increased risk (HR 2.98, 1.98-4.47), no evidence of interaction between the two risk factors could be detected.
Both increased adiposity and smoking are strong and independent predictors of disability pension, but they do not act synergistically.
Smoking behaviour has been monitored nationally through population surveys for 35 years in Canada, but these surveys have not been as consistent or rigorous as the magnitude of the smoking problem demands. Inconsistent methods and irregular survey intervals are just two of the characteristics that have made it difficult to know exactly how smoking is changing. Further, an absence of routine data on tobacco control policies (other than the price of cigarettes) has hampered understanding of the determinants of changing prevalence. The advent of two survey series--Canadian Tobacco Use Monitoring Survey (CTUMS) and Canadian Community Health Survey (CCHS) promises to change this situation for the better. We suggest that both are critical elements of a national smoking surveillance system and that, with a commitment to CTUMS in particular, Health Canada could set a new international standard for surveillance.