Environmental Health

The World Health Organization (WHO) defines health as ‘‘a state of complete physical, mental and social wellbeing and not merely the absence of disease or infirmity’’ (WHO, 1948). It is well recognized that the health of a population is influenced by a wide array of health determinants. Environmental and occupational determinants of health must not be considered in isolation, but rather in the broader context of genetic, biological, social, behavioral, and other health determinants, as interactions among them may produce synergistic or antagonistic effects.

The environment as defined in relation to health status is quite broad in scope, encompassing the natural environment (air, food, water, and soil), the built environment (including housing and the urban environment), and consumer products (such as household products and children’s toys). Although the influence of the environment on health status has long been recognized, it is often difficult to establish etiological connections between environmental exposures and specific adverse health outcomes for a number of reasons, including the multifactorial nature of many diseases, long latency periods, and cumulative and multiple exposures to environmental hazards. Small risks associated with low levels of exposure to environmental hazards can only be characterized with carefully designed studies of sufficient size.

Despite these difficulties, a wide range of adverse environmental and occupational health effects have been described, as will be seen in this article. Even small increases in risk can pose a substantial concern when considered on a population scale. A variety of scientific methods are used to evaluate environment–health outcome associations, including analytic epidemiologic studies, toxicological studies, and surveillance and biomonitoring programs.

Quantification of the burden of disease attributable to environmental factors allows for the prioritization of health intervention initiatives. Burden of disease estimates can vary considerably due to difficulties in quantification as well as uncertainties regarding causality. Worldwide, the WHO estimated that 23% of all deaths and 24% of the global disease burden is attributable to environmental factors. However, the environmental disease burden is not equally distributed, with 25% of all deaths in developing countries attributable to the environment, as compared to 17% in developed nations. Per capita, children in developing countries carry an eightfold greater loss of years of healthy life from environmental factors than children in developed countries. Clearly, low- and middle-income countries (LMIC) carry a disproportionate load of environmental disease burden. These differences were attributed to a number of factors including poor infrastructure, lack of sanitation programs, and vector-borne diseases in LMIC countries.

These observations clearly indicate that the environment exerts an important influence on health status. Fortunately, many environmental and occupational exposures are amenable to intervention. In implementing environmental health risk management programs, consideration must be given to population subgroups that may be particularly vulnerable to adverse environmental health effects. Public perception of risk must also be considered, as the success of any risk mitigation strategy can be affected by the public’s beliefs about the nature of the risk and their reaction to the intervention.

A Framework for Environmental and Occupational Health Risk Assessment

An integrated framework for population health risk assessment is presented in Figure 1 (Krewski et al., 2007). The framework integrates the concepts of population health and risk assessment/management within a common paradigm to facilitate the environmental health policy decision-making process. Prominent population health elements of this integrated framework are the determinants of health, which form its foundation. The influence of environmental and occupational factors is considered in the context of the broader array of determinants, including biology and genetic endowment as well as social and behavioral factors, and their interactions. Examining the broad range of determinants and their complex interactions is important to properly address critical population health risk issues by recognizing the full range of factors influencing health risk. A range of risk mitigation strategies are considered, ranging from regulatory to community action. Prominent risk assessment/management elements of the framework are health risk science, and health risk policy analysis; the latter component includes the selection and implementation of a risk management strategy, as well as the communication of information about the risk issue under consideration and the decision-making process. The remainder of this article will highlight key components of the framework, and provide an overview of adverse health effects associated with selected environmental and occupational health hazards.

Environmental Health Figure 1Figure 1. An integrated framework for risk management and population health. Reproduced from Krewski D, Hogan V, Turner MC, et al. (2007) An integrated framework for risk management and population health. Human and Ecological Risk Assessment 13(6): 1288–1312. Figure reprinted with permission of the copyright holder, Taylor and Francis Group.

Identification of Environmental and Occupational Health Risks

Toxicological and epidemiological investigations are two main approaches for identifying environmental and occupational health risks. Whereas epidemiological studies evaluate health risks in human populations, toxicological studies evaluate risks in the laboratory using a variety of in vitro or in vivo systems. Although epidemiological studies examine human health status directly, a variety of potential limitations can limit the strength of population-based investigations. On the other hand, toxicological studies are conducted in carefully controlled laboratory conditions, and can provide information on a range of health effects. However, results obtained in nonhuman test systems must then be extrapolated to the human experience.

Epidemiology

Epidemiological studies can range from simple case reports of adverse health outcomes in individual patients to highly complex analytic studies designed to assess specific associations between certain environmental contaminants and adverse health outcomes. Epidemiology is typically defined as the study of the distribution and determinants of disease in human populations. Last’s (2001) definition goes one step further, and explicitly states that epidemiology also involves the application of findings to health risk control. Therefore, simply describing environmental/occupational health associations is insufficient; rather, knowledge gained must be used in the design of the most appropriate risk management strategies to reduce the burden of disease.

Although case reports can provide clues about the causes of adverse health outcomes, these findings require confirmation in carefully conducted analytic investigations. Typically, case-control studies retrospectively collect detailed information on exposures of interest among a defined group of affected cases and an unaffected group of controls. In contrast, cohort studies collect exposure information on healthy participants at a defined entry point (or baseline) and follow cohort members over time for the occurrence of health outcomes of interest. Variants of these traditional study designs are also employed. The methodological strengths and weaknesses of these study designs are well described. A critical consideration with respect to environmental/occupational health for any epidemiological investigation is the availability of a precise and valid exposure metric.

Exposure may be defined using a variety of approaches including: self-reports (questionnaires, interviews), measures in the environmental media (routinely collected environmental monitoring data, study-specific measures), and measures of personal exposure (e.g., personal air samplers). Each of these exposure metrics represents only a proxy measure for the more relevant internal dose at the target tissue, which is largely not often practically or possibly measured. Exposure misclassification due to recall biases, difficulties in measuring exposure history in the distant past or in the most relevant etiologic period, and the choice peak or cumulative exposures as the most relevant exposure metric, can limit the strength of the investigation. Inter-individual variability in exposure from differences in personal behavior and toxicokinetic factors are also key methodological concerns. Occupational studies are typically faced with the difficulty of assessing risk from exposure to complex mixtures of contaminants that may vary over time, and are often forced to rely on job titles or records of employment as surrogate measures of exposure. Information on work behavior patterns including use of protective equipment is often difficult to obtain.

A range of technological advancements are being applied to environmental/occupational health issues to attempt to better characterize exposure history and reduce potential misclassification. In air pollution research, for example, the use of satellite data, geographic information systems (GIS) methodologies, land-use regression models, and studies of source apportionment may provide improved estimates of pollutant concentrations in ambient air. The use of computerized routines to link high-quality administrative databases on health status, such as cancer registries, mortality records, and hospital discharges or prescription drug use has also become a powerful tool in environmental epidemiology.

Other important analytic considerations limited power to detect subtle low-dose effects, additivity, or synergism among mixtures of pollutants, a lack of information on potential confounders or effect modifiers, and the classical ‘healthy worker effect’ in occupational and proportionate mortality studies. Nevertheless, analytic epidemiological investigations have been instrumental in elucidating a number of environmental/occupational health relationships such as radon and lung cancer, air pollution and adverse cardiovascular effects, and childhood lead exposure and cognitive defects.

Toxicology

Although toxicological investigations are conducted in nonhuman systems, they are of great importance in assessing potential environmental health risks as they can be performed in advance of the introduction of a substance into use, prior to any human exposure. Toxicity testing is a rapidly expanding field of scientific investigation, with the breadth of endpoints and sensitivity of tests available, particularly with the explosion of genomics, which is continually evolving. Toxicology and epidemiology are also interdependent disciplines, as the results of both are mutually considered when evaluating the weight of evidence for a specific environmental exposure/health outcome relationship. Such an integrated approach has been employed to advantage in the International Agency for Research on Cancer’s (IARC) monograph program.

Toxicological studies can range from acute studies that assess the toxicity of high doses of a substance in a short time frame with severe consequences, to subchronic and chronic studies designed to assess the effects of repeated exposures administered over a period of months or even years. Acute studies can provide information regarding the lethality of the exposure, whereas subchronic and chronic studies can provide information on endpoints requiring extended exposure, such as cancer.

Well-recognized limitations of toxicological approaches to heath risk assessment include uncertainties associated with extrapolation from animals to humans, the lack of availability of appropriate animal models for certain human diseases, and differences in exposure levels (human exposures are typically much lower than those evaluated in animal studies). Safety/uncertainty factors and mathematical risk models are typically applied to toxicological information for the purpose of establishing human exposure guidelines. A 100-fold safety factor has commonly been applied to the no-observed effect level for noncancer endpoints; this allows for a 10-fold difference in susceptibility between animal and human species, and a 10-fold difference in susceptibility among individuals in the human population. Additional safety factors may be applied to reflect the quality and completeness of the available scientific data. In the case of nonthreshold effects, mathematical modeling is sometimes used to determine a ‘virtually’ safe dose corresponding to a very low level of risk. The virtually safe dose is highly dependent on the slope of the dose–response curve, and is often estimated under strong assumptions, such as linearity of the dose–response curve at low doses. Recently, the benchmark dose (BMD) corresponding to a 5 or 10% increase in risk, has been proposed as a point of departure (PoD) for extrapolation to lower doses, with application to threshold and nonthreshold effects.

Toxicokinetic studies are used to describe the absorption, distribution, elimination, and excretion of xenibiotics. Physiologically based pharmacokinetic models are being increasingly used in risk assessment to estimate the dose of the reactive metabolite reaching target tissues. Toxicokinetic information is of value in designing appropriate testing protocols for new or existing substances, in interpreting the results from various toxicity tests, and in comparing results in different species.

In vitro testing procedures offer many advantages in terms of resource use. The Ames salmonella/microsome assay, introduced in the 1970s, remains one of the most widely used in vitro test procedures. The assay assesses the mutagenic potential of a particular substance by evaluating rates of reverse mutation in mutant bacteria strains deficient in their ability to synthesize histidine. Looking to the future, the U.S. National Research Council recently proposed a long-range vision for toxicity testing and assessment of environmental agents. Elements of the vision include: mapping of major toxicity pathways, greater use of computational toxicology to predict the toxic properties of environmental agents, the use of medium- and high-throughput in vitro test procedures to permit the assessment of a much greater number of environmental agents, and more use of cellular and molecular information derived from population-based studies.

Surveillance/Biomonitoring

The WHO defines surveillance as the ‘‘systematic ongoing collection, collation, and analysis of data and the timely dissemination of information to those who need to know so that action can be taken’’ (Last, 2001: 174). Awide variety of environmental/occupational health surveillance systems exist fromthe local/hospital level through to national and international levels. Surveillance systems can range from disease or outcome focused to product or risk factor focused. Injury surveillance systems, primarily outcome focused, have been established in many hospital systems throughout the world. Some focus on injuries in specific populations, such as children, whereas others seek to evaluate the injury profile among the whole population. Cancer registries provide another example of a well-established systematic, disease-focused, surveillance initiative. In contrast, surveillance systems related to adverse drug reactions or medical devices are based on a product-focused approach. Air-quality monitoring networks routinely collect data on the concentrations of specific air pollutants in certain geographic areas. Monitoring trends in disease or adverse outcome events over time can help to warn of emerging epidemics, and provide clues about possible etiological relationships.

In the context of environmental/occupational health, biomonitoring relates to the collection of biological samples, such as blood or urine, with which to measure levels of contaminants directly or indirectly through indicators of their physiological effects. Biomonitoring can be performed as part of an epidemiological investigation or as part of a routine surveillance program. Biomonitoring can offer a direct indicator of internal dose rather than relying on self-reported exposure measures and reflects cumulative exposure from all exposure routes. A range of contaminants has been examined in previous environmental health studies, including blood lead levels in relation to neurotoxic effects in children, and serum or plasma levels of PCBs (polychlorinated biphenyls) in relation to breast cancer risk.

Biomonitoring has recently revealed increasing levels of flame retardants in human breast milk. Limitations associated with biomonitoring include cost, the reflection of only recent exposures to nonpersistent chemical exposures, and the lack of information on the time course of past exposures.

Environmental Health Risks

Outdoor Air Pollution

The association between outdoor air pollution and a variety of disease outcomes including asthma, cancer, and cardiovascular disease has been extensively investigated. Since a number of air pollutants are ubiquitous in the urban atmosphere, it has been difficult to ascertain the specific source responsible for the observed effects. The WHO estimated that exposure to particulate air pollution is responsible for approximately 800 000 (1.2%) of total premature deaths worldwide. Region-specific estimates illustrate that air pollution is a greater risk factor for adverse health outcomes in developing countries, with developing Asia contributing approximately two-thirds of the global air pollution disease burden.

Short-term studies based on time series and related methods have revealed acute health effects including increased rates of heart attack, stroke, emergency room visits for respiratory symptoms, and overall mortality associated with daily levels of ambient air pollution. Specific subpopulations including the elderly, infants, and individuals with underlying illness appear to be at particular risk. Atmospheric pollutants have also been associated, although less consistently so, with various immunological, hematological, and reproductive outcomes.

Studies of the long-term health effects of elevated levels of air pollution have consistently reported positive effects. One of the largest investigations of the relationship between long-term exposure to ambient air pollution and mortality is that of the American Cancer Society. In Pope et al.’s (2002) analysis, each 10 mg/m3 elevation in fine particulate air pollution was associated with an approximate 4, 6, and 8% increase in risk for all causes, cardiopulmonary, and lung cancer mortality, respectively. The results from cohort studies investigating the health effects of long-term exposure to air pollution were used extensively in the development of air quality standards.

Indoor Air Pollutants

Radon

Epidemiological studies have established radon as a leading cause of lung cancer. Natural decay of uranium-238, a component of the earths’ crust, results in the release of radon-222 gas. Concentrations of radon are typically low outdoors, but can accumulate in enclosed environments. When inhaled into the lung, the short-lived decay products of radon can interact with biological tissues causing DNA damage. Although occupational case-control studies of uranium miners have consistently demonstrated a positive association between radon gas and lung cancer risk, the results of individual case-control studies of residential radon exposure have been less conclusive. To further evaluate the lung cancer risk associated with residential radon exposure, pooled analyses of case-control studies conducted both in Europe (13 studies) and North America (7 studies) were undertaken (Darby et al., 2005; Krewski et al., 2006). The North American pooling reported an excess odds ratio of 0.10 (95% confidence interval [CI]:-0.01–0.26) per Bq/m3 radon. Results from the European analysis were similar, with an 8.4% (95% CI: 3.0–15.8%) increase in risk of lung cancer per Bq/m3 radon reported. Overall, residential radon was estimated to be attributed to as much as 10% of lung cancer cases.

Other indoor air pollutants

A range of other indoor air pollutants have also been associated with specific adverse health outcomes in studies around the world. Cooking and heating with solid fuels on open fires or traditional stoves can contribute to high levels of indoor air pollution. This is especially relevant in developing countries, as many depend on solid biomass fuels (wood, charcoal, crop residues, dung) and coal for their energy needs. Biomass and coal smoke contain a large number of pollutants including particulate matter, carbon monoxide, nitrogen dioxide, formaldehyde, and polycyclic aromatic hydrocarbons such as benzo[a]pyrene. These pollutants were associated with increased risk of acute respiratory infection, chronic obstructive pulmonary disease (COPD), lung cancer, asthma, and adverse reproductive outcomes. A substantial body of evidence, particularly from China, has shown that women are especially at risk of developing lung cancer as a result of exposure to smoke from cooking with coal in their homes.

Other sources of indoor air pollutants include volatile organic compounds emitted from adhesives, carpeting, upholstery, pesticides, and cleaning products, outdoor air pollutants entering buildings through poorly located air intake vents and other openings, and moisture accumulation in building structures leading to high levels of bacteria and mold. Dampness in indoor environments may lead to various respiratory symptoms, asthma, and allergy (Laumbach and Kipen, 2005).

Drinking Water Contaminants

Safe and reliable drinking water is of paramount importance, as water is a basic biological necessity for life. Avariety of biological pathogens can threaten the integrity of the public drinking water supply, including bacterial, viral, and parasitic organisms. Gastrointestinal illness is the health effect most commonly caused by water-borne pathogens. Infants and the elderly are particularly at risk of severe illness and mortality from gastrointestinal illness. Sophisticated water treatment plants can typically limit the concentrations of biological pathogens to levels that do not pose a population health risk. However, disruptions in the water treatment process or unusual environmental events can lead to the occurrence of gastrointestinal disease outbreaks. In developing countries, poor infrastructure often results in chronic exposure to water contaminated with biological pathogens. This can lead to endemic gastrointestinal illness resulting in malnutrition and premature mortality. Surveillance systems designed to provide early warning signs of impending water quality issues are needed to implement risk mitigation strategies at the first indications of a problem, thereby preventing a large-scale outbreak.

Drinking water can also become contaminated with industrial discharges, pesticide residues, and leaching of natural occurring heavy metals due to acidification of the raw water source. The consequences of low-level chronic exposure to these compounds are not well established. Disinfection by-products in chlorinated drinking water are suspected in the development of several types of cancer, although the likely risks are low, particularly in comparison with the benefits of microbiologically mediated disease control. There is increasing concern surrounding the identification of excreted natural and pharmaceutical hormones in drinking water supplies. An association between long-term exposure to aluminum in drinking water and Alzheimer’s disease, a chronic neurodegenerative disorder, has been described; however, the evidence remains controversial.

Dietary Contaminants

Biological hazards

Individuals are exposed to a wide range of infectious or toxic compounds through the ingestion of food. Microorganisms are the source of a large proportion of food-borne illness globally. Some of the most common pathogens included salmonella, campylobacter, E. coli, and shigella. Poultry, red meat, unpasteurized milk, and untreated water are common sources of these organisms. Fresh produce can also become infected through the use of contaminated seeds, irrigation with contaminated water, and flooding. Food-borne illnesses of pathogenic origin typically result in gastrointestinal symptoms. These symptoms are usually short-lived and self-limiting; however, in a subset of the exposed population, they can cause severe health complications and risk of death, especially in the very young and very old. Long-term complications are rare, but include reactive arthritis from exposure to salmonella and shigella, Guillain-Barre syndrome from campylobacter exposure, and renal damage due to infection with pathogens such as E. coli O15H7. In industrialized countries, up to 30% of the population is affected by food-borne illness each year. The WHO has estimated that approximately 76 million cases of food-borne disease, resulting in 325 000 hospitalizations and 5000 deaths, occur each year in the United States. The global incidence of food-borne disease is more difficult to estimate due to a lack of surveillance and reporting systems in developing countries. However, over 2 million people are estimated to die from diarrheal disease each year, of which an appreciable proportion can be attributed to contamination of food and drinking water.

Chemical hazards

Toxic metals, PCBs, and dioxins can contaminate food through contact with polluted air, water, or soil. Pesticide residues and administration of pharmaceuticals to livestock can also result in chemical contamination of food. Persistent organic pollutants are fat soluble, and thus accumulate in the fatty tissue of fish and other animals over time. Residents in extreme northern climates are especially prone to highly persistent compounds that deposit in the region due to their long-range transport pattern through the atmosphere and subsequently bioaccumulate in the food chain. The health risks of persistent organic pollutants remain undefined, although certain types of cancer and adverse reproductive health outcomes are suspected.

Prions

Prions are unique pathogens with biological and physiochemical characteristics that differ significantly from those of other microorganisms. These agents arise from the conversion of a normal cellular protein into an abnormal disease causing isoform. Human prion diseases affect the central nervous system and fall under one of three etiological types: inherited, sporadic, or iatrogenic. Creutzfeldt-Jakob disease (CJD) is a rare and fatal brain disease in humans. The sporadic type, for which the cause is unknown, is the most common form of this disease, which mainly affects people aged 50 years or over. The annual incidence of human prion diseases is approximately one case per million. Despite the rare occurrence of these neurodegenerative disorders, considerable attention has been focused on prions because of their unique characteristics and concerns that major outbreaks of prion diseases in animals could lead to epidemics in the human population.

Bovine spongiform encephalopathy (BSE) is a transmissible brain disease of cattle characterized by progressive degeneration of the nervous system, first recognized in the United Kingdom in 1986. More than 184 000 cases of BSE were confirmed in the UK alone. The origin of BSE was linked to the inclusion of meat and bone meal contaminated with scrapie-infected (another prion disease) sheep parts in the feed of livestock, resulting in cross-species transmission. BSE has since been reported in numerous countries across Europe and North America. BSE, through exposure to contaminated meat, has been implicated in human disease – a variant form of Creutzfeldt- Jakob disease (vCJD). Since the first case of vCJD reported in 1996, nearly 200 patients with this disease have been identified worldwide.

Many countries have imposed cattle feed instructions, as recommended by the WHO, which prohibit the inclusion of most mammalian protein in feed supplies. Active surveillance programs to test for prions in high-risk cattle (those showing neurological symptoms or signs of sickness) have also been implemented to initiate mitigation measures at the first sign of infection.

Urban Environments

Densely populated areas present unique public health challenges. Crowded conditions combined with inadequate hygiene can result in the rapid spread of infectious disease. Increased infectious disease risk can also stem from inadequate solid waste collection resulting in an environment which favors the proliferation of vectors and reservoirs of communicable diseases. In tropical countries, these vector-borne diseases include malaria, dengue, and typhoid. In other climates, rodents and flies act both as mechanical and biological vectors of infectious diseases.

Individuals in many urban environments are exposed to high levels of air pollution as a result of heavy motor vehicle traffic and proximity to industrial complexes. Motor vehicle traffic also contributes to increased risk of injury from collisions and pedestrian accidents. It is estimated that 20 to 50 million people worldwide are injured or disabled each year due to motor vehicle accidents and that number is expected to rise, particularly in developing countries, due to rapid and unplanned urbanization (Peden, 2005). High levels of traffic noise have also been implicated in hypertension, sleep disturbances, and myocardial infarction. Despite these potential health risks associated with densely populated areas there are several advantages of living in an urban environment with respect to health including proximity to health-care facilities, public health programs, and increased opportunity to form social support networks.

Occupational Health Risks

Dangerous substances and conditions have always existed in the workplace. Historically, instead of improving such work conditions, there are accounts of ‘unhealthy’ work environments exploited as a form of punishment or of work relegated to lower classes. Since the effects of a toxic and unsafe work environment can be manifest in a wide variety of diseases and injuries, establishing a safe workplace has been an important population health goal in recent decades.

Carcinogens in the Workplace

From the first observations of Sir Percival Pott in 1775, associating scrotal cancer in chimney sweeps to deposits of soot, through to the modern era, carcinogens were first identified primarily in the workplace. Although this is no longer true, occupational cancer epidemiology remains essential to the discovery of cancer-causing agents in humans. The predominant source of evidence on human carcinogens has arisen from epidemiologic studies of highly exposed workers. Some early studies identified lung cancer risks in relation to suspicious occupational circumstances, such as nickel refineries, chromate manufacturing, and sheep-dip manufacturing. Concerted investigation of occupational agents came later, as exemplified by Sir Richard Doll’s 1955 quantitative assessment of the relationship between asbestos exposure and lung cancer risk. In recognition of the vast and growing body of evidence concerning environmental carcinogenesis, several programs were established in the 1970s to aid in governmental regulation, including the IARC monograph program and the Environmental Health Criteria monographs of the International Program on Chemical Safety within the WHO.

As of 2006, the IARC monograph program has identified 31 definite human occupational carcinogens, 29 probable carcinogens, and 116 possible carcinogens. A further 18 occupations and industries were identified that likely entail excess cancer risks, though the culpable agents have not always been identified. Table 1 provides a recent listing prepared by Siemiatycki et al. (2004) of occupational agents and circumstances identified as having strong evidence supporting a carcinogenic relationship with particular cancers. While some of the listed exposures are practically nonexistent in modern times, there are other exposures that are common worldwide. Exposure to crystalline silica, for example, is particularly ubiquitous, as is exposure to the many varieties of polycyclic aromatic hydrocarbons. Though the global burden of cancer attributable to occupational exposures is small, on the order of about 2%, Boffetta (2004) has argued that these cancers occur disproportionately among male blue-collar work populations, in whom occupational cancers may account for upward of 20% of cancers.

Respiratory Health

While the ‘dusty trades’ were linked to chronic bronchitis since the nineteenth century, it was recognized as early as the 1500s that lung disease was common in miners. The lung is particularly susceptible to occupational exposures such as airborne dusts and fumes. As shown in Figure 2, inhaled materials can increase the risk of virtually all of the major chronic lung diseases, with the exception of vascular illnesses. Allergens and irritants can cause sneezing and congestion. Particulate matter can be deposited to areas of the upper respiratory system, causing rhinitis and various bronchial illnesses. Exposure to chromic acid can cause nasal ulcerations. Irritants are commonly inhaled from common mixtures of bleaches and phosphorus or detergents and ammonia. Although COPD is primarily caused by smoking, chronic airflow limitations were related to exposure to silica, beryllium, cadmium (particularly emphysema), and cotton dusts (specifically bronchitis, or ‘brown lung’).

Table 1. Listing of occupational carcinogens and circumstances with strong evidence linking them to particular cancer sites

Environmental Health Table 1

Adapted from Siemiatycki J, Richardson L, Straif K, et al. (2004) Listing occupational carcinogens. Environmental Health Perspectives 112: 1447–1459 and Rousseau MC, Straif K, and Siemiatycki J (2005) IARC carcinogen update. Environmental Health Perspectives 113: A580–A581.

Environmental Health Figure 2

Figure 2. Occupational respiratory diseases. Reproduced from Becket W (2000) Occupational respiratory diseases. New England Journal of Medicine 342: 406–413.

Asthma has emerged as the principal occupational respiratory disease in industrialized countries. Hundreds of substances in the workplace are known to affect asthma, which can be categorized into occupational (new onset from workplace exposure) or work-aggravated (exacerbation of preexisting disease). The traditional definition of asthma referred to a reversible airflow limitation from sensitizing exposures. Recent consensus now also considers the existence of asthma from short-term, high-intensity exposure to irritants. The highest reported prevalence of occupational asthma has been found in the detergent industry, from exposure to platinum salts and proteolytic enzymes. Lombardo and Balmes (2000) list many of the major exposures that can induce asthma, such as various egg and animal proteins, grain dusts, flours, latex among health-care workers, proteases in the detergent industry, red wood dusts, and platinum salts.

Pneumoconiosis, a dust-related fibrotic lung disease, can be caused by inhalation of asbestos (asbestosis), silica (silicosis), iron filings (siderosis), and coal dust (black lung in coal miners). Silica exposure, in particular, is still a major concern among construction workers worldwide. Although there has been a decrease in the numbers of coal miners in Western Europe and North America, the numbers of miners remain large, particularly in Eastern Europe, India, China, Africa,Australia, and South America.

Occupational Radiation Exposures

Since its discovery by Roentgen in 1895, ionizing radiation has been exploited in medicine for diagnostic and therapeutic purposes. Historically, medical staff were occasionally exposed to sufficiently high doses to lead to skin burns. Indeed, the first substantial epidemiological evidence for the carcinogenic effects of radiation was obtained from observations on radiologists. International groups such as the International Commission on Radiological Protection were formed to provide recommendations for radiation protection for both workers and the public.

The discovery of nuclear fission in the 1930s led to the development of nuclear weapons, power industries, and subsequent occupational exposure to ionizing radiation. Underground rock miners can be exposed to high levels of naturally occurring radiation, from radon gas and its progeny, depending on surrounding uranium content. Other sources of exposure include workers involved with nuclear fuel production, reactor operation, irradiated fuel reprocessing, sterilization of medical products, luminizing, and radionuclide production. Studies of Japanese nuclear workers involved in weapon production during World War II, with high radiation exposure, were shown to be at excess risk of solid tumors in the lung, bone, and liver. Flight attendants can accrue high doses of cosmic radiation, and there are suggestions of excess melanoma and breast cancer. Cardis et al. (2005) provided recent evidence on low chronic exposures, indicating a small excess risk of cancer even at exposure levels consistent with current regulated standards. Fallout from the Chernobyl reactor failure in 1986 has recently been estimated to be associated with an additional 40 000 cases of cancer in Europe over the subsequent 80-year period (Cardis et al., 2006).

Pesticide Workers

Pesticides are a diverse family of chemicals. Health concerns are driven largely by the relative high toxicity of insecticides, nematicides, and fungicides. Exposure can occur by way of ingestion, inhalation, and skin absorption, with the latter two being the primary routes of exposure in worker populations. Although direct use of pesticides entails the highest exposure levels, such as in orchard and farm workers, even office workers are exposed to some extent when exterminators are present. Nosocomial poisoning is possible in health-care workers when handling patients with acute pesticide poisoning.

First used in chemical warfare, milder forms of organophosphates have since been formulated for use worldwide on agricultural crops and livestock. Used in preference to organochlorines, because of their safer environmental impact, many organophosphates have nevertheless been restricted by the Environmental Protection Agency (EPA). The WHO has estimated about 3 million cases yearly of acute pesticide poisoning, with the majority in developing countries in Africa, Asia, and Central and South America. With chronic exposure to low levels of organophosphates, a pesticide-related illness can develop, involving symptoms of nausea, headache, and vomiting. Additional long-term health problems were noted, including respiratory problems, memory disorders, neurological conditions, miscarriages, and birth defects. Pesticide workers also possibly have an excess risk of non- Hodgkin’s lymphoma, particularly linked to phenoxyacetic acid, organochlorine, organophosphate, carbamate, and triazine pesticides. As with many occupational exposures, complex analyses are needed to disentangle the individual effects of pesticides when workers tend to be exposed to multiple agents (see, e.g., De Roos et al., 2003).

Injury and Safety in the Workplace

The landmark U.S. Worker’s Compensation Act of 1911 established the need for safe working conditions. Workplace safety is an essential requirement for the modern worker. However, even with measures to reduce workrelated injuries and illness, safety concerns can still exist due to inadequate training and lack of compliance with safety regulations.

Workplace safety can be achieved in a number of ways. Guidelines have been established to limit ambient air concentrations of many occupational agents. In the case of pesticide workers, safety measures might include frequent changes of clothing, avoidance of eating in the workplace, and regulations regarding the use of personal protective equipment. Similar measures were implemented with medical staff, who are at constant risk of exposure to various pathogens from handling of patients and medical supplies.With the development of ergonomic measures to prevent musculoskeletal disorders, the reduction of falls, trips, and slips in the workplace has become an important goal for workplace safety. Reducing chronic noise exposure will not only prevent hearing loss, but may also have an influence on hypertension. However, research has also shown that introducing newer and safer equipment must also be accompanied by educational campaigns: improving risk awareness and compliance with safety measures, modifying work behavior, and reducing accidents by improvement of job skills.

Vulnerable Populations

Children’s Environmental Health

In contrast to the broader field of environmental health, children’s environmental health has come into prominence more recently. The National Research Council (1993) report, Pesticides in the Diets of Infants and Children, was a major stimulus in this regard. It reported that children may experience higher exposure levels to pesticide residues in food and a greater susceptibility, due to immature and rapidly developing systems, to their toxic effects as compared to adults. Regulatory changes embodied in the Food Quality Protection Act, including an additional 10-fold margin of safety, provided further protection for children against environmental exposures.

Among the leading causes of morbidity and mortality among infants and children, many have an appreciable environmental component. The weight of the evidence with which to characterize children’s environmental health issues can range from cases in which the evidence is substantive to cases in which the scientific basis for an association is limited or inadequate. The economic and societal costs associated with children’s environmental health disorders are estimated to be substantial, in part, due to the disruption of normal development with the potential for serious and irreversible consequences. Seemingly subtle adverse children’s environmental health effects from low-level exposures can be associated with large lifetime or population consequences (as is the case for lead).

Children may be exposed to potentially hazardous environmental agents through a number of pathways including ingestion, inhalation, and dermal; the developing fetus is exposed transplacentally to the mother’s body burden of environmental contaminants. Children’s exposures to environmental agents (adjusted for body weight) may exceed those of adults, thereby increasing the likelihood of adverse health effects, due to a combination of physiological and behavioral factors. Compared to adults, large differences in the consumption of certain foods and water per unit body weight are observed. Behaviors such as crawling, playing on the ground, and hand-to-mouth contact can increase the level of children’s exposure to environmental contaminants. Children may also be exposed to contaminants from parental occupational exposures from direct transfer from articles worn at work. Contaminants such as flame retardants, pesticides, plasticizers, metals, and therapeutic drugs were detected in the breast milk of women throughout the world, a food source unique to infants.

Complex patterns of growth and development are observed from conception through to adulthood. Development does not occur uniformly across each organ system, but rather through a series of stages of rapid development that occur at precise time intervals. These differential rates of development create critical exposure time windows that are characterized by periods of enhanced susceptibility to environmental exposures. The fetal and infant life stages are thought to be particularly sensitive to chemical exposures. Immature organ and tissue systems contribute to differences in the uptake, distribution, metabolism, and elimination of environmental agents in children, and may play important roles in increasing their susceptibility to the occurrence of an adverse health effect. Early life exposures also allow for an extended time period for the manifestation of delayed adverse health effects.

A particular challenge in the field of children’s environmental health is that the majority of established relationships in population studies are those where high levels of exposure were observed. Considerably less is known regarding chronic low-dose exposures to which the majority of the pediatric population is exposed. The effects of such low exposures are particularly difficult to characterize in epidemiological studies, resulting in uncertainty about the nature and level of potential health risk. As noted in the following section, genetic and socioeconomic factors may affect children’s susceptibility to exposure to environmental hazards.

Gene–Environment Interactions

Many human diseases are believed to result from an interaction between genetic susceptibility and modifiable environmental factors. Gene–environment (GE) interactions reflect differences in the effects of environmental exposures among individuals with different genetic polymorphisms. Differences in genetic susceptibility can render some individuals in a population to be more or less likely to develop a particular disease following exposure to an environmental agent. Elucidating GE interactions has been particularly difficult, requiring considerable understanding of the biological underpinnings of human disease. Large-scale epidemiologic studies specifically designed to evaluate GE interactions are just beginning to be conducted.

Xeroderma pigmentosum is an autosomal recessive disorder in which exposure to ultraviolet (UV) light results in a high incidence of skin cancers, due to defective DNA repair; although skin cancer can occur from UV light exposure without this genetic disorder, the risk of UV-induced skin cancer is much greater among individuals with this genetic condition. Simple GE interactions, where the exposure and the gene are both well understood, are rare in environmental/occupational health. Most diseases likely involve a complex profile of multiple genes, lifestyle factors, and environmental exposures. Studies have suggested several possibilities of potentially vulnerable populations, though they are yet to be fully understood. There is evidence that asthma has a number of environmental and occupational etiologies; several candidate genes were identified with suggestive evidence implicating interactions with isocyanate exposure, smoking, and ozone exposure with antioxidant supplementation. Parkinson’s disease is believed to have some association with agricultural pesticides, and, given that there are dramatic differences in the reported prevalence in different countries, a complex multigenic interaction has been suggested. Psychiatric disorders, such as depression and schizophrenia, have long been suspected of having genetic susceptibilities that moderate the effects of environmental determinants. Inflammatory diseases like rheumatoid arthritis have recently been studied, with conflicting results suggesting that smoking history is a trigger for the release of rheumatoid factors in the presence of certain alleles of the human leukocyte antigen. Squamous cell carcinomas of the oral cavity, pharynx, and larynx have also recently been studied to understand what, if any, interaction exists between tobacco smoke and polymorphisms of several carcinogen-metabolizing enzymes.

Environmental Health Risk Issues

A wide variety of environmental/occupational health risks have so far been described. The WHO has estimated that globally, diarrhea, lower respiratory infections, other unintentional injuries (a category distinct from road traffic injuries), and malaria, represent the greatest opportunities for interventions to reduce the burden of environmentally mediated disease. A variety of policy options are available for managing such health risks. Policies aimed at directly improving environmental quality may be used alone or in combination with policies aimed at improving environmental health indirectly through social, behavioral, or other interventions.

Public Perception of Risk

Public perception of risk is an important factor in environmental/ occupational risk management decision making. Risk perception is a subjective or intuitive process by which individuals evaluate the probabilities and consequences of risks. As such, public perceptions of risk often differ from quantitative or expert determinations of health risk. Discrepancies in risk apprehension between the public and health authorities can lead to challenges in risk communication and undermine the effectiveness of risk mitigation strategies.

Since zero risk from exposure to an environmental/ occupational contaminant may often be unattainable due to reasons of feasibility or cost, the level of risk that society should be willing to assume or tolerate has been debated. Specification of a precise level of risk that might be considered acceptable in some sense is, however, problematic (Hrudey and Krewski, 1995).

Public perceptions of risk and acceptable levels of risk are influenced by a wide range of factors. Studies of risk perception conducted throughout the world have identified a number of individual- and population-level characteristics related to level of risk perceived. Risk perceptions are influenced by demographic factors such as gender, age group, level of educational attainment, and income; personal values and beliefs; as well as personality traits such as locus of health risk control. Population-level factors are also related to risk perceptions, particularly the nature and type of media exposure and the credibility of the source. Specific characteristics of the hazard, particularly factors related to the degree to which it is dreaded and understood, also influence risk perceptions. A hazard, for example, will tend to be dreaded, and thus, perceived as a greater threat, if the consequences are fatal, globally distributed, affect future generations, or for which the individual may be involuntarily exposed. Concern surrounding a hazard will also be increased when the risk is new or unknown to science, or for which levels of exposure are difficult to quantify. Industrial sources of radiation, such as nuclear power plants, as well as environmental chemical contaminants, such as pesticides, are examples of such hazards that consistently appear in the risk perception literature. Understanding of public perception as risk issues evolve will aid in the development of effective risk mitigation programs.

Risk Management

A wide range of mitigation strategies are available for environmental/occupational health protection including regulatory, economic, advisory, community action, and technological approaches. Such mitigation strategies may be employed jointly or separately according to the nature of the environmental/occupational health scenario of concern. Evaluation of any strategy following its implementation is required to assess its impact on environmental/ occupational health status. It is also important that any risk management strategy be equitable and responsive to the availability of new scientific data.

  • Regulatory action is often used by governments at multiple levels to mitigate health risks. Regulatory action for environmental/occupational health protection is often required under differing conditions of uncertainty. Whereas there exists a considerable amount of scientific evidence to support regulations governing the use of lead in a variety of consumer products, for other potential environmental hazards – such as the cosmetic use of pesticides – municipalities that have banned their use have done so in a predominantly precautionary view as the body of scientific evidence supportive of adverse health outcomes remains limited.
  • Economic approaches to mitigating environmental/occupational health risks typically make use of economic incentives or disincentives to control the level of population exposure to environmental contaminants. For example, emissions trading effectively places an economic burden on polluters while rewarding those who reduce emissions.
  • Advisory approaches may include information campaigns related to behavior change, such as advisories related to the consumption of sport fish or the need to boil water due to the presence of a known or suspected biological contaminant, or labeling of products to ensure their proper use and disposal.
  • Community involvement in environmental/occupational health risk management can include such factors as resource mobilization, information sharing, priority setting, shared decision making, and implementation of selected initiatives. Community action has resulted in policy change, such as bans related to cigarette smoking in public areas.
  • Technological options for health risk management such as engineering advancements, may be employed, for example, to reduce population levels of exposure to environmental contaminants or reduce level of risk associated with certain activities or occupations. Technological approaches including improvements in road design and in automobile safety features are widely employed in the prevention of road traffic injuries.

Emerging Environmental Health Issues

Environmental/occupational health risk issues continue to evolve and emerge over time. Emerging pathogens, such as the virus responsible for avian flu in Europe and Asia, have had significant impacts on international trade. This initial experience with avian flu challenges us to find new ways of anticipating and preventing similar outbreaks in the future, including a possible outbreak of pandemic flu. The threat of terrorism has prompted major efforts to address the chemical, biological, radiological, and nuclear risks associated with such potential terrorist events. Little is known about the potential risks of emerging technologies such as biotechnology and nanotechnology, which can be expected to play an increasingly important role in the future. Endocrine toxicants were associated with adverse effects on the ecological environment and animal species and are suspected to play a role in a variety of human diseases.

Human activity has also resulted in global change, including climate change and impacts on biogeochemical cycles, which are expected to impact the biosphere far into the future. Population health risk issues related to climate change include the impact of extreme weather events, heat stress, health effects of particulate and gaseous co-pollutants associated with greenhouse gas emissions, increased cancer risks due to increased exposure to UV radiation, and the migration of infectious disease-carrying insect vectors. The full extent of such impacts is currently being evaluated by governments throughout the world and by international agencies with responsibilities for both population health and the environment.

Current evidence clearly indicates that environmental/ occupational factors impact population health status. Scientific investigations will continue to uncover new linkages between our environment and human health, and refine current understanding of existing environmental health risks and their interactions with other health determinants, particularly social and genetic factors. Government, academia, industry, and nongovernmental organizations will need to work together to assess and manage known environmental and occupational health risks and respond to new risk issues as they emerge. International collaboration will be essential in addressing transboundary and global risk issues. The approaches to risk assessment and risk management outlined here may be of value in meeting this challenge.

Bibliography:

  1. Becket W (2000) Occupational respiratory diseases. New England Journal of Medicine 342: 406–413.
  2. Boffetta P (2004) Epidemiology of environmental and occupational cancer. Oncogene 23: 6392–6403.
  3. Cardis E, Vrijheid M, Blettner M, et al. (2005) Risk of cancer after low doses of ionising radiation: Retrospective cohort study in 15 countries. British Medical Journal 331: 77.
  4. Cardis E, Krewski D, Boniol M, et al. (2006) Estimates of the cancer burden in Europe from radioactive fallout from the Chernobyl accident. International Journal of Cancer 119: 1224–1235.
  5. Darby S, Hill P, Auvinen M, et al. (2005) Radon in homes and risk of lung cancer: Collaborative analysis of individual data from 13 European case-control studies. British Medical Journal 330: 223.
  6. De Roos AJ, Zahm SH, Cantor KP, et al. (2003) Integrative assessment of multiple pesticides as risk factors for non-Hodgkin’s lymphoma among men. Occupational and Environmental Medicine 60: E11.
  7. Hrudey SE and Krewski D (1995) Is there a safe level of exposure to a carcinogen? Environmental Science and Technology 29: 370A–375A.
  8. KrewskiD, LubinJH, Zielinski JM, et al. (2006) A combined analysis ofNorth American case-control studies of residential radon and lung cancer. Journal of Toxicology and Environmental Health Part A 69: 535–597.
  9. Krewski D, Hogan V, Turner MC, et al. (2007) An integrated framework for risk management and population health. Human and Ecological Risk Assessment 13(6): 1288–1312.
  10. Last JM (ed.) (2001) A Dictionary of Epidemiology. New York: Oxford University Press.
  11. Laumbach RJ and Kipen HM (2005) Bioareosols and sick building syndrome: Particles, inflammation, and allergy. Current Opinion in Allergy and Clinical Immunology 5: 135–139.
  12. Lombardo LJ and Balmes JR (2000) Occupational asthma: A review. Environmental Health Perspectives 108(supplement 4): 697–704.
  13. National Research Council (1993) Pesticides in the Diets of Infants and Children. Washington, DC: National Academy Press.
  14. Peden M (2005) Global collaboration on road traffic injury prevention. International Journal of Injury Control and Safety Promotion 12: 85–91.
  15. Pope CA III, Burnett RT, Thun MJ, et al. (2002) Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution. Journal of the American Medical Association 287: 1132–1141.
  16. Rousseau MC, Straif K, and Siemiatycki J (2005) IARC carcinogen update. Environmental Health Perspectives 113: A580–A581.
  17. Siemiatycki J, Richardson L, Straif K, et al. (2004) Listing occupational carcinogens. Environmental Health Perspectives 112: 1447–1459.