Introduction to Environmental and Occupational Health
Environmental and Occupational health (“EOH”) refers to the role of environment and occupation on human health. This is a branch of public health. The field of study helps us to answer the following questions:
(1) What is “environment” in environmental health?
(2) What is meant by “hazards” and “risks”?
(3) What is referred to as “exposure” and “dose”?
(4) What are the three branches of study in Environmental and Occupational Health?
(5) How are studies of Epidemiology, Toxicology, and Environmental Health Risk Assessment relate to each other?
(6) How can we manage environmental and occupational health risks?
What is “Environment” in Environmental Health?
Note that occupational health is a special case of environmental health and refers to health issues associated with jobs occupations, professions, and in the context of work. This is why here we will discuss occupational and environmental health together as “Environmental Health”.
When we study environmental health, our aim is to understand the role of environment in shaping our health and what can we do about it. For example, if we know that exposure to air pollution leads to respiratory diseases such as asthma, then, in order to prevent asthma, we will need to improve air quality. If we know that if the quality of our drinking water is poor and leads to diarrhoeal diseases, then, we must improve our drinking water standards and take steps to prevent such illnesses. Therefore, in the discussion of environmental health, environment refers to an element we can modify to improve public health.
What do we mean by “environment” in Environmental Health?
Hence, we mean by “environment” that is both:
(1) External to humans and
(2) Results from human activities.
For example, environmental tobacco smoke is an environmental health issue. Smoke from cigarettes results in air pollution; inhaled smoke also leads to different illnesses. Smoke from burning cigarettes drifts in air and reaches our air passages. Smoke results from human activities (smoking); smoke is external to us; and, smoking harms our health. Hence smoking is an environmental health problem.
In contrast, health effects that result from earthquake cannot be labelled as an environmental health problem even though severe physical and mental health issues result in people who suffer consequences of earthquakes. The reason health effects of earthquake cannot be described as environmental health is that there is no reason to believe that earthquakes are results of human activities, and consequently there is nothing we can do to prevent earthquakes. For example, Kario et.al. (2003) noted,
Earthquakes provide a good example of naturally occurring acute and chronic stress, and in this review we focus mainly on the effects of the Hanshin-Awaji earthquake on the cardiovascular system. The Hanshin-Awaji earthquake resulted in a 3-fold increase of myocardial infarctions in people living close to the epicenter, particularly in women, with most of the increase occurring in nighttime-onset events
Source: Kario K, McEwen BS, Pickering TG. Disasters and the heart: a review of the effects of earthquake-induced stress on cardiovascular disease. Hypertens Res. 2003 May;26(5):355–67. (https://www.ncbi.nlm.nih.gov/pubmed/12887126)
Because earthquake is a natural disaster, not a human engendered event, hence heart disease resulting from being exposed to earthquake is considered as a response to a natural disaster, rather than an “environmental health” problem. The decision here is driven by whether something is “human engendered” or not. The idea being, if you were to be certain that something is “human engendered”, then you can think of mitigating or preventive action to address the resulting health effects. This is important for prevention and has public health consequences.
It may seem that the distinctions are not obvious. For example, natural disasters such as storms and hurricanes result in significant health effects such as infectious diseases and people getting injured, yet we will label health impacts from hurricanes and storms as health effects from natural disasters rather than environmental health issues. But we also know that increased frequency of storms and natural disasters are results of global warming, and global warming is human-engendered or “anthropogenic” (e.g. “What is the link between hurricanes and global warming?”). From this viewpoint, we can argue that health effects resulting from people being exposed to storms and natural disasters are “environmental health” problems, and that if we can reduce global warming, this will affect the frequency of “storms and hurricanes” and in turn will have implications for human health issues resulting from “natural disaster induced health problems”.
Another point of distinction is that, for a health problem to be labelled as environmental, the trigger should always be external to humans, they cannot come from internally or inside of humans. This implies that pathological effects resulting from gene mutations or changes in the “internal milieu” are not considered “environmental”. For example, a gene mutation results in several chains of transformations leading to breast cancer. The mutation or the gene is inside the body and not external to the body. We can argue that certain food or exposure to toxins result in this mutation and therefore this mutation should be environmental as in altering the cell environment, but this is beyond the scope of “environmental health”.
Other than these two specifications, you can interpret environment in many ways. For example, physical environment (air quality and pressure, pressure changes such as sea diving or flying, or being exposed to radiation), chemical environment (working in factory floor with toxic fumes, air pollution, or drinking polluted water), psychosocial environment (workplaces where rude employers, or work conditions with very little control of how much work you can do but a lot of responsibility or job demand) and so on. So, while the scope of environment being defined is quite broad, it is important to keep in mind the narrowness of the scope of defining that, it has to do with how humans are responsible for the environmental factors to arise and that it is always external to the person concerned.
Hazard versus risk: which is which?
We are exposed to “agents in the environment” that can harm our health. For example, we are exposed to particulate matters in the air we breathe, or many different chemical and biological contaminants in the water and food we consume. Almost everywhere and in all our activities through many other sources, we are exposed to substances that can impact our health. Although all of these are “potentially” harmful, it depends on the amount we are exposed. Any entity in the “environment” that can potentially harm our health is referred to as a “hazard”.
For example, a glass of water, about 300 millilitre, can be both beneficial AND harmful. Consumed in normal quantities of 1.5 litres every day for most healthy people, we need water for health. On the other hand, if we were to consume say 3 litres of water per day, we might end up with symptoms of over-hydration and damage our kidneys. In this sense, water can be BOTH healthful and harmful, depending on the amount we consume. This concept, that a substance that can be BOTH beneficial AND harmful depending on the amount consumed is an important learning point in environmental health and in toxicology.
Parcelsus (1493–1541) famously stated that the dose is the poison (sola dosis facit venenum). This statement forms the basis of toxicology. Everything can be hazardous. Just as a pothole in middle of the road can be hazardous if people step into it, but not otherwise, air can be hazardous if people inhale the toxic particulate matters, but not if people wear gas masks so that they do not inhale the toxic elements; water can be hazardous if people drink too much, or if people fall in a pool, not otherwise. Hazard is the possibility of harm. In this sense, hazards are qualitative statements, and we consider any entity as a hazard if we can demonstrate that they have a potential to cause harm. We can also state that
hazard is a likelihood of an event that can happen at time point t + delta (delta= a gap) t provided that it has not occurred till a time point t.
Risk refers to the result once hazard is realised. Cigarette smoke can damage lungs; therefore cigarette smoke is a hazard. The risk of cigarette smoking is lung disease (among other diseases) and we can state that risk only after we find evidence that cigarette smoking is associated with lung cancer. An open hole in a road is a hazard. Fracture of leg is a risk of that hazard. According to the American Cancer society, “Smoking shortens male smokers’ lives by about 12 years and female smokers’ lives by about 11 years”. Here “reduction of life span” is the risk.
Exposure and dose
In order that the hazards can result in risks, humans must be “exposed” to the “hazard”. For example, polluted air can cause asthma. For that to happen, our lung tissues must come in “contact” with contaminants in polluted air; if we do not come in contact, or if we can break the contact with the pollutants, then the health effects will not result. If we wear protective devices to keep out the contaminants or if we can take other precautions to keep out the contaminated air, then although the air is hazardous, we will be safe as we are not “exposed” and the risk will not accrue.
Exposure, therefore, is a qualitative concept. The amount we are exposed to and the amount that comes in contact with the part of the body that is affected is the dose. The amount of the contaminant that comes in contact with the tissue on which it interacts with is the “dose”. If the dose is low, even with exposure, the harm may or may not occur. Dose therefore refers to the amount of the toxin that reaches the target organ ready to exert its effect. So, the pathway goes something like
hazard is present in the environment → we are exposed through an exposure pathway → dose of the hazard inside the body comes in contact with the tissues → exerts its action → the body acts on the hazardous object or its transformed products → health effects accrue (0r the body responds) → the risk
As we see in the above pathway, a hazardous object in the environment enters the body through exposure pathways, and exerts an effect on the tissue(s) when sufficient quantities of it accrue or are present.
In toxicology, the action of the agent/toxin on the body and its “movement” is toxicokinetics of the toxin. The body, in turn, acts on the agent/toxin and will metabolise, store, or eliminate it. That action of the body on the toxin is referred to as toxicodynamics of the body on the toxin. A balance between the toxicokinetics and toxicodynamics of the toxin and the body determines the health effects.
Environmental epidemiology refers to the study of distribution and determinants of diseases in populations; where determinants are in the environment. As we move from hazard to risk, we traverse two parallel paths: first, we must identify the hazard and second, in parallel, we must characterise the risk.
For example, a slippery pavement (say one that has “black ice” on it) is a health hazard: people can slip and break their hips. Ralis (1981) conducted a study on icy pavements and risk of hip and other bone fractures in Cardiff, Wales in 1981; he studied patients who reported with fractures resulting from fall from walking on icy pavements on days when it snowed and compared it with what he termed as control periods or chosen days when it did not snow and calender days a year later. The following graph shows the results:
From this graph we see that for adults 31–60 years, snow and ice days had 272% more fractures that were reported to the hospitals than that in the control days (sunny days and days when they did not have snow and ice). For people aged 61 years and above, you can see that 214% more fractures were reported in the snow and ice days. These figures suggest that snow and ice days that result in icy pavements are risk factors for hip fractures and therefore icy pavements are hazardous to health.
Question: Can you think of how the human element in modification of environment comes into consideration of how people can slip and fall on icy pavements?
In environmental epidemiology, we study environmental factors as exposure and we compare people with and without specific health states or people with and without specific exposure and then compare exposure or health states. Based on the findings of the studies we build the evidence on the linkage between environmental factors and health effects. Hence epidemiology is critical for environmental and occupational health in testing explanations and theories that underlie the observations we make.
For example, in 1980s, doctors in India observed many patients who reported with signs of dark and white pigments in their palms and on their hands. Many of these patients were people who worked in farms and had for years consumed water they pumped from the ground using shallow tube-wells (for the skin disease they reported see the following figure):
The doctors suspected that the patients with these lesions must have been exposed for a long time to inorganic arsenic, and to confirm their diagnoses, they ordered urine tests for these patients. As they suspected, urine samples tested positive for inorganic arsenic for these patients. They found that contamination of groundwater with inorganic arsenic that they obtained from tubewells was the source of exposure. The researchers also compared the levels of inorganic arsenic in the drinking water of those people who were similar but who did not have skin diseases using an epidemiological study design referred to as “case control study”. They found that people who had skin diseases had higher levels of inorganic arsenic in their drinking water, and the higher the concentration of inorganic arsenic, the higher was the likelihood that these people would end up with arsenic-caused skin lesions. From these and other investigations, they identified that inorganic arsenic was the cause of these skin lesions among these farming and rural community inhabitants. This helped them to establish public health programmes to reduce or eliminate arsenic from the drinking water.
Environmental Health Risk Assessment
What happens when we identify that X is a hazard by conducting epidemiological studies? The next step is to quantify the risk. That process is referred to as “Environmental health risk assessment”. This is a stepwise process consisting of four sequential steps:
- Step 1: Identify the hazard. This can be done with epidemiological studies or laboratory animal and tissue studies.
- Step 2: Assess exposure. Exposure assessment is about toxicology.
- Step 3: Characterise the dose response relationship (Step 3, “Dose Response Assessment”). We assume that the higher the dose of an agent at the point of action in the body, the more intense will be the outcome, and hence important for risk.
- Step 4: using data from exposure assessment and dose response, characterise the risk and decide at what exposure level, the risk is likely ot be minimum. If we know the extent to which a person is exposed to the hazardous agent, or entity, and if we know the nature of the dose response curve or dose response relationship, then we can ascertain the or we can characterise the risk.
For example, we know that emissions from factories and cars, and burning of fossil fuels will lead to particulate matters and gases that will harm our health. This is the step of identification of hazards. Often such identification can be inferred from studies in human tissues; other times from animal experiments. Once a health hazard is identified, then the next step is to ascertain how much of it we are exposed to in our environment. For example, daily measurement of air quality is an indicator of how much of the air pollution we are exposed to on a daily basis. This step is referred to as “Exposure Assessment”. The exposure is not only on the outside environment, but also on the basis of molecules or compounds that we believe will accrue as a result of the exposure. For example, in case of air pollutants, we can sample from inhaled air how much of the particulate matters enter the body. In step 3, we ascertain the dose-response relationship.
We assume as dose of the exposure increases, so does the likelihood of “effect” or health effect. The relationship can be both linear (left hand side of the figure), and non-linear (right hand side figure).
If we know the level of exposure (that is if we can ascertain how much we are exposed to the hazardous agent), consequently the “dose” of the toxin, and the nature of the dose-response effect, we can characterise the resulting health risk.
How do we manage environmental health risks?
Public health professionals need to devise ways they can minimise hazards and mitigate health risks. For this reason, they need to use frameworks. Frameworks provide a plan of action. We will discuss here the DPSEEA framework (“Driving force — Pressure — State — Exposure — Effect — Action”, see the following figure).
As can be seen in the figure, driving force refers to those “forces” in the environment that has led to the emergence of the hazard. For example, consider the various ways we humans have changed our physical environment since the beginning of industrial age (scholars refer to this period as “anthropocene”). Our uses of technology and production of waste, burning of fossil fuel and generation of plastic waste have changed the environment. These changes are referred to as “driving forces (D)”. The “driving forces” that change the environment put “pressure” on the environment. To continue with this example, industrial activities have resulted in increased greenhouse gas emissions. Each time we put “pressure” on the environment, these pressures change the “state” of the environment. For example, before the industrial age, the level of greenhouse gases in the stratosphere was low, but with industrial activities, the level of the greenhouse gases in the stratosphere continued to increase. This is referred to as “change of state”. In turn, such “state changes” lead to emergence of new “exposures” for humans. So with the change in state of greenhouse gases in the stratosphere, we see increase in global temperature. Such exposure results in health effects.
Once we are able to recognise the driving forces, pressures they exert on the environment, the state change that results from the forces, the exposure that results from that change of state, and the health effects that result from the exposure — we can plan action to mitigate the health effects. This is the ‘action’ (A) of DPSEEA. This action can be taken at multiple levels: starting with changing in the driving force (so that we can aim at reduction in fossil fuel production) to developing technology or other means to reduce pressure on the environment (such as using “carbon sinks” or planting forests), to aiming to reverse the state (develop weather warning systems and move people away from coastal areas), to reducing exposure (building better heat proof homes), to improving adaptation and resilience. Often these need to be done together.
- Environment in Environmental health refer to human engendered sources of alteration of our surroundings that in turn would affect our health. While there are other sources such as genetic or natural causes that could also impact our health states, environmental health would only refer to the human-caused changes in our “environment” that would affect our health states. This distinction is needed as in public health, our aim is to promote health and prevent illnesses. If we were to identify the root cause as human activities, then this knowledge would provide us with a way to address the root cause of the health problem.
- Any entity in the environment (that conforms to the definition of environmental health) that is capable of causing harm to our health is termed as hazard. This concept of hazard is qualitative. Once we identify a hazardous entity in the environment, we can avoid it. However, human illnesses or health states that occur as a result of interaction with the hazardous entity is risk, and risk is always quantified.
- Interaction with the hazardous entity occurs in two phases: (1) we would need to come in direct “contact” with the hazard or be opened up to the hazard: a state we call “exposure”, so we will have to be “exposed” to the hazard and (2) after we are exposed, a certain amount or level of the exposing agent must be in contact with our tissues or selves so that it can exert its action. That amount or level is referred to as “dose”. The “dose” is the poison according to a fundamental concept of toxicology.
- The hazard and the dose and the responses to the dose of exposure are studied using Environmental Epidemiology. Environmental epidemiology is that branch of epidemiology where the determinants are in our environment. Many different study strategies are adopted by the environmental epidemiologists to to identify and quantify hazards and risks: ecological studies, case series or surveillance, cross sectional surveys, case control studies, cohort studies, and intervention research such as randomised controlled trials.
- If we know the hazards, then for communities and workplaces, we can conduct environmental health risk assessment. This is a four step process where (1) we identify the hazard in the first place, (2) we measure the level of exposure and the dose that humans come in “contact” with the exposure or hazard, (3) ascertain the relationship between the dose and the associated health effect and (4) and on that basis, characeterise the risk as to how many individuals are at risk.
- If we know the hazard, the exposure route, the health risk, then it behooves us to mitigate the risk. This is best done by frameworks, and DPSEEA (driving force, pressure, state change, exposure, effects and action) is a framework that enables addressing the environmental health problem.