Attention is increasingly given to environmental factors such as chemical exposures on the job as a cause of CVD, but often the medical community ignores this area of research and focuses on individual lifestyles. While overeating, lack of exercise, and smoking greatly increase one's risk of heart disease, so do stress and exposures to toxic substances on the job. Prevention should not only focus on what individuals do to themselves, but should also focus on what is beyond the individual's control -- the workplace.
Risk factors associated with coronary heart disease (CHD) can be divided into three categories: personal, hereditary, and environmental. Personal risk factors include sex, age, race, high serum cholesterol (most specifically low-density lipoprotein (LDL)/cholesterol ratio), high blood pressure, and cigarette smoking. The interaction between these factors is strong enough that a smoker with high blood pressure and hypercholesterolemia is eight times more at risk of developing CHD than a nonsmoker who has normal blood cholesterol and normal blood pressure.
Other personal risk factors, such as obesity, diabetes, and lack of physical exercise have been associated with CHD, but their roles are considered minor compared with those cited above. In certain families, the risk of CHD is high and is correlated with the number of blood relatives who have developed the disease and the early age at which they developed it.
Recognizing that cardiovascular health problems can be caused by chemical, physical, and/or psychosensory agents in the workplace, OCAW members in a variety of industries have voiced strong concern over the role of job exposures in the development of heart disease. Continuing to raise the issue ; will insure that the occupational health community direct its research efforts at work-related CHD. Simply put, we need more studies.
The small node in the upper chamber of the heart activates this recycling process. This node regulates the heart to a rate of 60 to 80 beats per minute. The node sends out an electrical impulse that causes the heart muscle to contract and, as the muscle tightens, it compresses the blood-filled chambers to force blood out through the heart valves.
Clinical disorders cause this node to send out inappropriate impulses. These abnormal impulses and other changes in the heart muscle or its impulse conducting system can result in abnormal heart rhythms (arrhythmias). Unless corrective measures are taken to restore the normal heart rhythm, these arrhythmias can reduce the pumping ability of the heart.
When the blood enters the smallest capillaries of the circulatory system, it supplies every cell in the body with oxygen and nutrients, and removes carbon dioxide and other materials from these cells. When the blood enters the lungs, it picks up fresh oxygen and gives up its accumulated carbon dioxide. While the heart provides the body with its essential blood supply, it also circulates a small percentage of its output through the heart's own blood vessel system, the coronary arteries.
Diseases which cause the blood vessels to corrode and to deteriorate are called cardiovascular diseases. They cause more deaths annually than all other causes of death combined.
Coronary arteriosclerotic heart disease (CAHD) or hardening of the arteries is the most common of diseases affecting the cardiovascular system and one which has been linked with environmental exposures.
CAHD is a disease in which the inner linings of the arteries are thickened and roughened by deposits of fat, fibrin (a clotting material), cellular waste, and calcium. These deposits interfere with the smooth flow of blood and the amount of blood carried through the artery. Clots form early leading to heart attack or stroke.
When inhaled, CO combines with hemoglobin, the oxygen- carrying substance in the blood, and forms carboxyhemoglobin. By replacing oxygen, CO deprives tissues of the necessary oxygen for survival.
In individuals with heart problems, low level exposure to CO has been shown to intensify the problem and may accelerate atherosclerosis or hardening of the arteries.
Few studies of worker populations exposed to CO have been conducted, but there is some evidence that stationary engineers and firemen at power plants have an increased frequency of death from heart disease. Steam boilers at these plants pose a potential exposure problem. However, the association between chronic exposure to low levels of CO and the development of coronary atherosclerosis leading to CHD has yet to be shown. Recent literature indicates that low exposure to CO accelerates the development of atherosclerosis in laboratory animals when combined with a diet rich in saturated fats, especially when exposure consists of intermittent peaks.
The few studies conducted so far among working groups have been unable to show a distinct relationship between chronic exposure to CO and the development of CHD. The known association of CHD with cigarette smoking, combined with recent observations that workers intermittently exposed to peaks of CO have higher risk of heart disease, keeps this question open to further research.
The Permissible Exposure Limit (PEL) for nitroglycerin is .2 parts per million (ppm) and for ethylene glycol dinitrate is .05 ppm.
Studies have reported elevated risk for CHD after some 20 years of exposure, which seems to indicate that nitro compounds are not only responsible for acute vasospastic reactions but may also increase the risk of CHD after long exposure by an increase in high blood pressure and atherosclerosis.
Although CS2 is primarily known for its toxic effects on the central nervous system, it also causes hardening of the arteries in both animals and humans. One study of deaths among male workers found that exposed workers had twice the incidence of heart disease as workers with no exposure to CS2.
CS2 has also been linked with high blood pressure or hypertension in exposed workers.
The current OSHA exposure limit of 20 ppm for CS2 is inadequate for worker protection since NIOSH recommends 1 ppm of carbon disulfide.
Studies have shown that geographical areas with soft drinking water have an increased incidence of heart disease. The explanation for this is that soft water is corrosive and dissolves metals and trace elements that contribute to heart disease. Their dissolution means that instead of sifting out, you ingest the metals in drinking water.
Much of the research done on hydrocarbons concerns their ability to cause abnormal heart rhythms or arrhythmias. Concerns over the toxic properties from inhaling nasal decongestants containing 1,1,1 trichloroethane led to a ban on the chemical's use in decongestants.
In addition, some researchers have proposed that noise can also damage the cardiovascular system indirectly by causing high blood pressure. Over a long period of time, this may lead to atherosclerosis of the heart and blood vessels. Intermittent and impact noise would seem to be more harmful than continual noise in this respect. However, reports have been rather inconsistent on this issue and observations are frequently confounded by problems in testing procedures.
Acute exposure to high levels of noise initiates cardiovascular responses that mimic the effects of acute stress: these include increases of blood pressure and heart rate; changes in blood levels of catecholamines and lipids, such as low-density lipoproteins and fatty acids; as well as vascular tone of peripheral vessels. These changes are transitory, however, and disappear a short time after exposure ends. Long-term effects of exposure to noise, such as chronic high blood pressure, coronary atherosclerosis, or ischemic heart problems have yet to be demonstrated.
In most North American workers' compensation programs, CHD is considered to be an injury caused by accident rather than an occupational disease. The presence of an accident originally meant that some "unusual exertion" was a necessary precondition, but its definition varied much with time and place.
It is reasonable to assume that most courts of law will accept cases when four conditions are met: 1) the asserted heart pathology is well demonstrated; 2) the CHD has followed an exertive activity, not encountered normally in the execution of the work (often this is in relation to an emergency situation); 3) the heart attack took place immediately or in a reasonable period of time after the effort; and 4) a physician states that the exertion, more probably than not, triggered the attack.
There seems to be a general agreement that fire fighters and policemen are at high risk for CHD and, accordingly, several states have favorably considered compensation cases for these workers. The impetus for such an attitude has been a concern over the physical and emotional stresses of both occupations, and in addition, the chemical hazards encountered in fighting fires.
2. If your members work with any of the substances listed in this Alert, start a log of who suffers heart disease, the type, and the age and job classification of the member. Safety stewards in each department can be responsible for the log for that department.
3. If you feel you have an excess of heart disease in the plant or a particular department, contact your International Representative. He or she will work with the Health and Safety Department to determine whether conditions warrant a NIOSH Health Hazard Evaluation.
Published by the Oil, Chemical and Atomic Workers International Union, P.O.Box 281200, Lakewood, CO 80228-8200, April 1994.