Health Effects

In the preceding sections, we outlined the complex intertwined ways in which environmental conditions and agents and animal health co-evolve. In this section we describe the frameworks used to characterize the effects of various environmental agents on health. “Health effects” is the general term that describes the effect of an agent (microbe, chemical, environmental conditions) on health. These effects are described and characterized in terms of disease rates (morbidity) or death rates (mortality).

Health effects are discussed in terms of population health. Thus we may talk of the occurrence of so many diseases per 100,000 people. The science of studying public health was first developed to study epidemics of infectious diseases such as typhoid, cholera and diseases among certain occupational groups, such as cancer among chimney sweeps in London. This field of study is called epidemiology.

Health effects are generally studied systematically using a framework shown in Figure 2. It is a cause and effect model where one looks at the effects as arising from exposure to an agent, being influenced by various life factors (genetic and lifestyle), and manifesting in disease. As we are talking of public health, the factors in the figure and the total model are treated statistically.

Numerous interactions affect each stage of the exposure-effect process. The “agent in a medium” refers to the primary agent (chemical, virus, infections) that lives in or is carried by a medium. Examples are the malaria sporidia in the mosquito vector (or in the water); or, the carbon monoxide or sulfur dioxide in air. Various conditions – swampy water close by, weather and wind patterns – of the natural environment affect the exposure. Environment here includes the socio-economic and overpopulated conditions. The activity profile includes the activities that bring people within reach of the agent and those that might enhance the action of the agents. These could be positive activities such as exercise or negative ones such as smoking and other health-related aspects such as diet and previous exposure. They also include occupational activities that may be associated with exposure directly or indirectly.

Exposure is measured or characterized in ways that include the amount of agent (e.g., the amount of CO per liter of air) and the pattern that causes the agent to enter or affect the body – breathing or intake rates, as well as genetic or other predisposing factors.

“Other exposures” refers to those from lifestyle (alcohol, tobacco, hormones and pesticides in food, vitamins in food) and from the environment that may interact with the primary exposure and aggravate or ameliorate the effects.

The exposure then causes cellular or tissue level effects, which may or may not be cumulative. If the body can metabolize and excrete the agent, the effects may not occur or may be different than if the agent accumulates, especially in organs such as lungs and liver, which are “cleansing” organs. The cellular level effects then may build over time either with continuous exposure or with intermittent exposure.

When a foreign chemical enters the body, it gets absorbed and processed in different ways. Figure 3, adapted from Human Physiology: The Mechanisms of Body Function by Vander, Sherman, and Luciano (McGraw Hill, 2004), shows a scheme of the metabolic pathways of a foreign chemical.

The processes shown in Figure 3 cumulatively contribute to disease. The action of the agent may be site-specific. For example, lead, which is chemically similar to calcium, deposits in the bones; iodine deposits in the thyroid gland, which is the body’s iodine processor. It has been found that certain synthetic chemicals such as the pesticide DDT (mentioned earlier in the section on malaria) and the drug DES (diethylstilbestrol, given to pregnant women to prevent miscarriage) are hormone mimics or endocrine disruptors. The body metabolizes them as if they are the female hormone estrogen. This causes serious damage to developmental and reproductive processes. DDT has been shown to make eggshells fragile, and DES causes vaginal cancer in children when they become teen-agers. As the effect was delayed significantly from the time of administration, and happened in a person other than the one who took it, the discovery of the effects and the banning of DES happened years after its use began.

When the body does not metabolize a chemical, it may end up deposited in fatty tissue or the liver. PCB’s (polychlorinated biphenyls) an industrially useful synthetic chemical, is one that does not break down in the environment or in the body. This family of “persistent” chemicals were introduced in 1929 and used for numerous applications – cooling fluids in transformers, as lubricants, cutting oil, and in paints, varnishes, inks and pesticides – and became ubiquitous in the environment. It has even spread to very remote “pristine” areas.

About 50 years after its use began, it was everywhere. PCB’s tend to deposit in the liver and fatty tissue. Scientist Theo Colborn says that they “might be found virtually anywhere imaginable: in the sperm of a man tested at a fertility clinic in upstate New York, in the finest caviar, in the fat of a newborn baby in Michigan, in penguins in Antarctica, in the bluefin tuna served in a sushi bar in Tokyo, in the monsoon rains falling in Calcutta, in the milk of a nursing mother in France, in the blubber of a sperm whale cruising in the South Pacific, in a wheel of ripe brie cheese, in a handsome striped bass landed off Martha’s Vineyard on a summer weekend. Like most persistent synthetic chemicals, PCB’s are world travelers.” (Our Stolen Future, p. 91-92)
Persistent chemicals can also bioaccumulate and biomagnify as they work their way up the food chain. Figure 4, from Our Stolen Future (p.27) shows how the small amounts in plankton cumulate up through the food chain, becoming a million times more concentrated in the bird.

Figure 4: As PCBs work their way up the food chain, their concentrations in animal tissue can be magnified up to 25 million times. Micorscopic organisms pick up persistant chemicals from sediments, a continuing source of contamiantation, and water and are consumed in large numbers by filter feeding tint animals called zooplankton. Latger species like mysids then consume zooplankton, fish eat the mysids, and so on up the food wev to the herring gull. (Figure and caption from Our Stolen Future, p. 27)

Metabolic transformation, persistence, and bioaccumulation are therefore three ways in which synthetic chemicals that we have not evolved with and become part of our ecology cause their effects.

The absorption and various metabolic processes and depositions thus become steps that result in disease. For example, liver cancer is a long-term effect of PCB exposure. In order to be able to characterize and manage the effects, various frameworks have been evolved. One used most often is risk assessment. We now discuss the basic principles of risk assessment and risk analysis.

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