Cardiovascular Diseases Clinical Trial
To assess the risk of cardiovascular mortality in workers with increased occupational exposure to carbon monoxide.
BACKGROUND:
A retrospective study by NIOSH found a significantly higher death rate from atherosclerotic
heart disease for New York City tunnel officers compared with the expected rate for the New
York City population. A Cox proportional hazards model which examined the risk of
atherosclerotic heart disease for tunnel officers compared to bridge officers found a
similar pattern. The Cox model also showed a significant decline in the risk of
atherosclerotic heart disease among tunnel officers, when compared to the less-exposed
bridge officers, after cessation of exposure with most of the risk dissipating within as
little as five years.
Carbon monoxide may contribute to cardiovascular disease through several accepted and
potential mechanisms including binding to hemoglobin, and reducing oxygen dissociation at
the tissue level by shifting the oxygen-hemoglobin dissociation curve. Carbon monoxide in
experimental animals also increases platelet stickiness which may contribute to
atherogenesis, and accelerates atherosclerosis either through altered lipid metabolism or
increasing vessel permeability to cholesterol. Carbon monoxide in experimental studies
contributes to sudden death by reducing the cardiac threshold for ventricular fibrillation.
Some of these mechanisms, such as those that would lead to transient hypoxia of the
myocardium, would lead to increased risk of myocardial ischemia only when exposure is
current, while other mechanisms, such as acceleration of atherogenesis, may lead to long
standing elevation of risk for cardiovascular disease.
The Occupational Safety and Health Administration standard for carbon monoxide in 1987
allowed exposure of 50 parts per million (ppm) time-weighted average over an 8-hour day with
no ceiling level limit. The margin of safety of this standard for workers with
cardiovascular disease was questioned by a series of controversial studies of exposures
averaging 50 ppm which demonstrated a decrease in exercise necessary to induce angina in
experimental subjects with underlying cardiovascular disease. NIOSH recommended a standard
for carbon monoxide exposure of 35 ppm as an 8-hour time-weighted average with a ceiling
limit of 200 ppm.
DESIGN NARRATIVE:
For each study site, personnel records were obtained including a work history for each
exposed worker. For current workers, smoking history was obtained by questionnaire and
carboxyhemoglobin measured both pre-shift and post-shift. The feasibility of obtaining
smoking history on previously employed workers was explored. Vital status ascertainment
included the use of records from the Social Security Administration, drivers license
bureaus, the Internal Revenue Service, and the National Death Index. Death certificates were
obtained from appropriate state vital statistics offices. Statistical analyses were
performed using a modified life table analysis system frequently used by National Institute
of Occupational Safety and Health (NIOSH) in similar studies. In addition, industrial
hygienists from NIOSH visited each study site to measure current occupational exposure
levels and to gather information which allowed estimation of past exposure levels. Previous
carbon monoxide monitoring data was available for some tunnels.
Based on the results of the cohort study, a nested case-control study was planned to further
examine the interaction of smoking and other cardiovascular disease risk factors with the
relationship between cardiovascular disease and occupational exposure to carbon monoxide.
The study completion date listed in this record was obtained from the "Completed Date"
entered in the Query View Report System (QVR).
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