Dataset Information

Analysis of air pollution mortality in terms of life expectancy changes: relation between time series, intervention, and cohort studies.

ABSTRACT:

Background

Information on life expectancy change is of great concern for policy makers, as evidenced by the discussions of the so-called "harvesting" issue (i.e. the question being, how large a loss each death corresponds to in the mortality results of time series studies).

Methods

Whereas most epidemiological studies of air pollution mortality have been formulated in terms of mortality risk, this paper shows that a formulation in terms of life expectancy change is mathematically equivalent, but offers several advantages: it automatically takes into account the constraint that everybody dies exactly once, regardless of pollution; it provides a unified framework for time series, intervention studies and cohort studies; and in time series and intervention studies, it yields the life expectancy change directly as a time integral of the observed mortality rate.

Results

Results are presented for life expectancy change in time series studies. Determination of the corresponding total number of attributable deaths (as opposed to the number of observed deaths) is shown to be problematic. The time variation of mortality after a change in exposure is shown to depend on the processes by which the body can repair air pollution damage, in particular on their time constants. Hypothetical results are presented for repair models that are plausible in view of the available intervention studies of air pollution and of smoking cessation. If these repair models can also be assumed for acute effects, the results of cohort studies are compatible with those of time series.

Conclusion

The proposed life expectancy framework provides information on the life expectancy change in time series studies, and it clarifies the relation between the results of time series, intervention, and cohort studies.

SUBMITTER: Rabl A

PROVIDER: S-EPMC1373624 | biostudies-literature | 2006 Feb

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Analysis of air pollution mortality in terms of life expectancy changes: relation between time series, intervention, and cohort studies.

Rabl Ari A

Environmental health : a global access science source 20060201

<h4>Background</h4>Information on life expectancy change is of great concern for policy makers, as evidenced by the discussions of the so-called "harvesting" issue (i.e. the question being, how large a loss each death corresponds to in the mortality results of time series studies).<h4>Methods</h4>Whereas most epidemiological studies of air pollution mortality have been formulated in terms of mortality risk, this paper shows that a formulation in terms of life expectancy change is mathematically ...[more]

PMID: 16451722

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Project description:Zinc (Zn) is a major elemental component of respirable ambient particulate matter (PM) detected often at alarming levels in urban air. Exposure to PM has been widely associated with increased cardiovascular morbidity and mortality, however, it is not known what components or sources of PM are causative. We recently demonstrated that long-term episodic inhalation of combustion PM, having similar amount of Zn found in urban PM, caused myocardial lesions in rats. We further demonstrated that a single pulmonary exposure to Zn at high concentration is associated with disturbances in cardiac mitochondrial function, ion channel regulation, calcium homeostasis, and cell signaling. Therefore, in this study we investigated the role of PM-associated Zn in cardiac injury using multiple exposure scenarios. Male Wistar-Kyoto (WKY) rats of 12-14 wks age were intratracheally exposed (once per wk x 8 or16 wks) to either (1) saline (control); (2) PM having no soluble Zn; (3) combustion PM suspension containing 14.5 ug/mg water-soluble Zn at high and (4) low dose levels, (5) the aqueous fraction of this suspension devoid of solid insoluble particulate fraction (14.5 ug/mg soluble Zn), or (6) Zn sulfate. Zn concentrations were identical in groups 3, 5 and 6. Pulmonary toxicity was apparent in all exposure groups when compared to saline as determined by recovery of cells in bronchoalveolar lavage fluid. Long-term exposure to PM with or without soluble Zn, or Zn sulfate caused distinct myocardial lesions characterized by subepicardial and randomly distributed myocardial inflammation, degeneration, and fibrosis. The lesion severity was higher in those groups receiving Zn PM. Because cardiac mitochondria are likely the primary target of inhaled metal or other absorbed PM components, we analyzed mitochondrial DNA damage using QPCR and found that all exposure groups except those exposed to PM without Zn caused variable degree of damage. Aconitase activity, sensitive to inhibition by oxidative stress was inhibited slightly but significantly in rats receiving zinc sulfate. Although modest, microarray (Affymetrix) analysis revealed expression changes in the heart reflective of effects on cell signaling, inflammation/oxidative stress, mitochondrial fatty acid metabolisms and cell cycle regulation in rats exposed to zinc sulfate. However, these changes were minimal following exposure to PM devoid of soluble metals. We demonstrate that episodic subchronic pulmonary exposure to zinc sulfate causes cardiac injury and mitochondrial DNA damage. Thus, water-soluble PM-associated zinc may be one of the PM components responsible for cardiovascular morbidity. Experiment Overall Design: Group 1 received Saline to serve as a control. Group 2 received Mount St. Helenâs ash, which does not contain any water-soluble zinc or other metals such that we can delineate any cardiac effect secondary to pulmonary deposition of these particles as these fine mode particles themselves are not likely to translocate to the heart. Group 3 received whole saline suspension of the same fugitive oil combustion particle sample used in the previous study, which contained insoluble components plus water-soluble zinc (Kodavanti et al., 2003; 14.5 ug/mg zinc) and also a small amount of water-soluble nickel (3.0 Âµg/mg). Elemental composition of this PM is comparable to Ottawa urban PM (Kodavanti et al., 2003). Group 4 also received same particle sample but at half the dose than group 3. Group 5 received saline-soluble or leachable fraction of PM-HD devoid of any solid material but contained soluble components including zinc and nickel. And, group 6 received zinc sulfate at concentration that was present in groups 3 or 5. This design allowed us to test if cardiac injury in rats was due to leached of zinc or solid particles. There were 4 replicates per treatment group.

Dataset Information

Analysis of air pollution mortality in terms of life expectancy changes: relation between time series, intervention, and cohort studies.

Background

Methods

Results

Conclusion

Publications

Analysis of air pollution mortality in terms of life expectancy changes: relation between time series, intervention, and cohort studies.

Similar Datasets

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