How Government Health Agencies Obscure the Impact of Environmental Pollution and Perpetuate Reductionist Framings of Disease: The Case of Leukemia

Abstract

Since the 1970s, environmental health researchers have documented environmental pollution's impacts on human health, which includes the bioaccumulation of industrial chemicals and how these toxicants contribute to disease. However, the relationship between disease and pollution is often difficult to discern in the disease information provided by dominant institutions. Previous scholarship has identified that print media, television news, online medical publishers, and medical associations consistently obscure the environmental causation frame. However, less has been said about disease information provided by public health agencies. To address this gap, I analyzed the leukemia information provided by Cancer Australia, the United States’ National Institutes of Health, and the United Kingdom's National Health Service. My analysis shows that the disease information offered by these health agencies also obscures the environmental causation frame by failing to identify most toxicants that environmental health researchers have linked to leukemia and by emphasizing a biomedical framing of the medical condition. Beyond documenting the problem, this article also discusses the social consequences and sources of the problem.

Since the 1970s, environmental health researchers have produced a growing literature showing that exposure to industrial chemicals contributes to disease, often in subtle but profound ways.^1–4 This relationship holds for immunological problems, reproductive issues, birth defects, musculo-skeletal problems, cancers, metabolic disorders, and most other disease categories. ⁵

Yet, in contrast to the growing environmental health scholarship, social scientists have found that the disease information disseminated by dominant institutions tends to obscure the relationship between disease and pollution. For instance, scholarship has shown how industries seek to obscure the relationship by using suppression, denial, downplaying, and/or distraction.^6–9 Social scientists have documented similar problems with other dominant institutions, such as mainstream media^10–12 and, to a lesser extent, the medical profession.^4,13

The circulation of deficient information matters because it can significantly shape the citizenry's understandings of disease, including what it is, what causes it, who is responsible for causing it, how it should be treated, and how it can be prevented. If a citizenry believes that environmental pollution contributes to disease, they will be incentivized to mobilize against pollution production. On the other hand, if the citizenry is led to believe that a disease is caused by defective genes, the focus will be on obtaining adequate treatment.

A type of institution that has been underanalyzed is government health agencies. This gap is particularly important because such agencies have an implicit and sometimes explicit mandate to prevent disease. To address this gap, I analyzed the leukemia information provided by public health agencies in three countries: (a) Australia's Cancer Australia, (b) the United Kingdom's National Health Service (NHS), and (c) the United States’ National Institutes of Health (NIH).

My analysis reveals that while environmental health researchers have identified 18 toxicants and toxicant classes that have a solid association with leukemia, the link between toxicants and leukemia is obscured by all three public health agencies. Additionally, it illuminates the methods through which health agencies obscure toxicant information and discusses the public health, social justice, and economic consequences of doing so. Lastly, I discuss sources of the problem, with a particular focus on the dominant medical paradigm and political economy.

How Dominant Institutions Frame Disease

As Clarke (2006) argues, all diseases are recognized and experienced within a social and cultural context. ¹⁵ In contemporary Western democracies, an important shaper of that context are dominant institutions (such as mass media, online medical publishers, and medical associations) that communicate disease information, as they play a central role in shaping what is known about a disease and influencing how disease gets addressed.

Frame analysis is a potent way of shedding light on these issues as it focuses attention on which information is provided, which is excluded, and the ramifications that flow from the choices. Entman (1993) defines framing as: “to select some aspects of a perceived reality and make them more salient in a communicating text, in such a way as to promote a particular problem definition, causal interpretation, moral evaluation, and/or treatment recommendation”. ¹⁴ (p.52). Clarke (2006) specifies that three widely used frames for discussing health information are medical, lifestyle, and political economy. ¹⁵ A medical frame portrays disease as biologically based pathologies that can be traced to malfunctions in the human body, such as malfunctions with organs, cells, or genes. A lifestyle frame attributes disease to harmful activities, such as smoking, consuming alcohol, or eating fatty foods. A political economy frame relates disease to the social context within which bodies are located, which includes the pollution that bodies are exposed to, as well as the economic and political systems responsible for that pollution. Whereas the first two frames situate disease in the individual, a political economy frame situates disease in the social context within which that body resides.

Previous scholarship has found that dominant institutions consistently favor medical and lifestyle frames over the political economy frame.^10–13,16 What makes this development increasingly pertinent is that environmental pollution has become particularly problematic in recent decades. Although industry-based pollution has been a significant problem since the nineteenth century, the problem has qualitatively worsened since World War II, due to the increased production and use of plastics, chemical pesticides, and other non-biodegradable chemicals. ¹⁷ Scholars estimate that over 80,000 chemicals are used in the United States and that 2,300 new ones are brought to market each year.^1,18 The problem is worsened by the fact few have been properly tested for safety. For instance, only 7 percent of the 3,000 high-volume chemicals (i.e., chemicals surpassing 1 million pounds per year) used in the United States have been properly tested for safety. ¹

The growing use of chemicals has increasingly polluted our air, water, and soil, which has led to toxicant bioaccumulation in human tissues. Biomonitoring studies reveal that U.S. citizens have, on average, 91 industrial chemicals in their bodies.^19,20 Additionally, the Environmental Working Group found over 200 industrial chemicals in the umbilical cord blood of each newborn they analyzed, which highlights that toxicant exposure starts in the womb. ²¹

In turn, the growing contamination of human bodies has led to disease. For instance, Houlihan and colleagues (2003) found that bioaccumulated toxicants are linked with particular medical problems, with U.S. citizens carrying, on average, 53 carcinogenic chemicals, 62 that are toxic to the brain and nervous system, 58 hormone-disrupting chemicals, 55 associated with birth defects, and 53 that harm immune systems. ¹⁹ Moreover, these problems are particularly concerning for the poor and communities of color, who, due to discriminatory siting of polluting facilities, are most likely to live near sources of pollution.^22,23

Given the extensive list of health problems linked to toxicants, one would expect that dominant institutions committed to human well-being, such as government health agencies, would feature toxicants prominently in the disease information they publicly disseminate. In particular, one would expect them to identify all toxicants substantially linked to the medical condition, routes through which people can be exposed to the chemicals, and what communities can do to protect themselves from such exposures. For example, information about seizures should alert readers to: (a) the numerous toxicants that are solidly linked to seizures, including lead, mercury, carbon monoxide, methyl bromide, and organophosphate pesticides ²⁴ ; (b) how people, especially children, can be exposed to those toxicants; and (c) what communities can do to ensure that their living environments (including work, home, and recreational) are free of those toxic threats.

However, dominant institutions tend to ignore or downplay toxicant information, focusing instead on biological dysfunctions and lifestyle choices.^10,11,25 For instance, in their groundbreaking work on the topic, Brown and colleagues (2001) revealed that print media consistently obscures and downplays the relationship between toxicants and breast cancer, emphasizing instead the role of genes and lifestyle choices. ¹¹ Likewise, a follow-up study by Atkin and colleagues (2008) revealed that toxicant risk factors were mentioned in only 4 percent of breast cancer stories in print and television media. ¹⁰ Lewison and colleagues (2008) found a similar result with the BBC website's coverage of breast cancer. ¹⁶ Moreover, Vallée (2020) found a similar pattern with online medical publishers, as WebMD's coverage of leukemia ignored most toxicants related to the condition and downplayed the role of those they did name. ¹³ Beyond mass media, similar problems exist with information provided by the medical profession. For example, Steingraber (2009) found that cancer educational materials distributed in clinics, hospitals, and waiting rooms failed to mention relevant toxicants. ⁴ Likewise, Vallée (2013) found that the 2011 U.S. clinical practice guidelines for Attention Deficit Hyperactivity Disorder failed to mention lead, manganese, polychlorinated biphenyls, or other toxicants linked to the syndrome. ¹²

Such information deficiencies matter because they obscure the harm that can occur when people are exposed to industrial chemicals, which makes it more difficult for the public to be aware of the problem, let alone mobilize to address it.

Although previous scholarship has examined mass media, online medical publishers, and the medical profession, to my knowledge, no one has similarly analyzed disease information provided by government health agencies. This matters for several reasons. First, for those with reliable internet access, government information is readily accessible, due to it being free, accessible on-demand, and accessible from a distance. Second, government information tends to be quite influential because of the authority people typically confer to government health agencies. Third, government agencies have resources to substantially increase the rhetorical effectiveness of their messaging. Fourth, given that taxpayers are funding them and they have a mandate to prevent disease, such agencies have a moral duty to provide cutting-edge environmental health knowledge so that communities can better protect themselves from preventable disease.

Methods

To address the gap in scholarship, I analyzed the leukemia information provided by Cancer Australia, the United States’ NIH, and the United Kingdom's NHS. I focused on these cases because they were the only health agencies in Anglophone countries (i.e., countries where English is natively spoken by the majority) that provided dedicated webpages for leukemia. At the time of this analysis, no similar webpages exist for Canada, Ireland, or New Zealand.

Leukemia is a blood cancer that involves the bone marrow and lymphatic system. It has four subtypes: (a) Acute Lymphocytic Leukemia (ALL), (b) Chronic Lymphocytic Leukemia (CLL), (c) Acute Myelogenous Leukemia (AML), and (d) Chronic Myelogenous Leukemia (CML).

One reason for focusing on leukemia is that it is a medical condition that is strongly linked to numerous toxicants, including benzene, pesticides, formaldehyde, 1,3-Butadiene, and ionizing radiation (see next section for more details). Another is that it impacts numerous people. Each year, there are an estimated 3,900 new diagnoses in Australia, 9,907 in the United Kingdom, and 60,000 in the United States, with most of these people undergoing significant medical treatment.^26–28 Additionally, leukemia contributes to significant mortality, with an estimated 2,029 deaths predicted for Australia in 2022, 4,830 for the United Kingdom, and 24,000 for the United States. Moreover, it is, by far, the leading cause of cancer among children under 15 in all three countries.^29–31

There is also evidence suggesting that leukemia is unequally distributed. For instance, Hispanics in the United States have had consistently higher rates of pediatric ALL. ³² Moreover, U.K. data shows that socioeconomic deprivation increases mortality rates among AML patients, with those in most the deprived quintile having a 50 percent higher mortality rate than those in the least deprived quintile (see Table 1). ³³

Table 1.

Leukemia Statistics by Country.

	United States	United Kingdom	Australia
# of new leukemia cases per year	60,650	9,907	3,900
New diagnoses per day	166.2	27.1	10.7
Incidence rate	14.1 per 100,000	18 per 100,000	16 per 100,000
Leukemia's rank among cancers	11th	12th	11th
% new cancer cases from leukemia	3.2%	3.0%	3.3%
# deaths from leukemia each year	24,000	4,830	2,029
# leukemia deaths per day	65	13	5.5
Mortality rates from leukemia	6.1 per 100,000	9 per 100,000	6.1 per 100,000
% of cancer deaths from leukemia	3.9%	3.0%	3.9%
Leukemia's rank for cancer deaths	6th most common cause of cancer death	12th	8th

Sources: ^{26–28,34–36}.

My study, which had two parts, consisted of analyzing how the health agencies framed leukemia. The first part focused on tracking the health agencies’ coverage of toxicants that environmental health researchers have substantially linked to leukemia, as specified in the next section. While I looked for toxicant coverage on the home page and all other webpages linked to it, I was particularly interested in the coverage provided on the “Risk Factors” page as that would be a particularly salient place for health agencies to provide information about toxicants linked to disease.

The second part consisted of reviewing the webpages for statements where leukemia was attributed to genes and/or lifestyle factors (such as smoking). As emphasized by Brown and colleagues (2001) and Vallée (2020),^11,13 framing a condition in reductionist terms can undermine environmental causation frames and, thus, has to be part of the analysis.

Environmental Health Scholarship on Leukemia

The environmental health research community has three authoritative bodies that track the relationship between toxicant exposure and cancer: the International Agency for Research on Cancer (IARC), the Collaborative for Health & Environment (CHE), and California's Office of Environmental Health Hazard Assessment (OEHHA). I relied particularly on the first two because they provided information that was specific to leukemia. Below I provide a brief summary of IARC and CHE, after which I discuss the toxicants that are strongly linked to leukemia.

IARC is the World Health Organization's specialized cancer agency. It was founded in France in 1965 to reduce humanity's growing cancer incidence by promoting international collaboration in cancer research. ³⁷ The agency focuses on identifying how lifestyle and environmental risk factors interact with genetics to produce cancer. This focus implicitly recognizes that “most cancers are, directly or indirectly, linked to environmental factors and thus are preventable”. ³⁷ One of the agency's key contributions has been the IARC Monograph Program, in which international working groups evaluate the carcinogenicity of toxicants and publicly disseminate their findings.

The CHE was founded in 2002 to create an interdisciplinary research network on environmental health issues. ³⁸ A significant contribution has been the Toxicants and Disease database, ⁵ which enables users to identify all toxicants associated with a disease and, conversely, all diseases associated with a particular toxicant. Additionally, the database signals the strength of evidence for each implicated toxicant.

In recent decades, environmental health researchers have linked leukemia to numerous toxicants. As seen in Table 2, CHE identifies five toxicants with a “strong” amount of evidence linking it to adult-onset leukemia. A “strong” designation means “a causal association with the disease has been verified” and is recognized by the scientific research community. ³⁹ CHE also lists 13 other toxicants or toxicant classes as having a “good” level of evidence, which is the designation for “toxicants associated with a disease through epidemiological studies (cross-sectional, case-series, or case-control studies) or for toxicants with some human evidence and strong corroborating animal evidence”. ³⁹ Below I discuss toxicants that are strongly linked to leukemia.

Table 2.

Toxicants That are Associated with Adult-Onset Leukemias.

Strong Evidence	Good Evidence
1,3-butadiene	1,2-dichloroethane
ethylene oxide	Agent Orange
formaldehyde	alachlor
ionizing radiation	aromatic amines
Benzene (acute non-lymphocytic leukemia)	arsenic
	carbon disulfide
	carbon tetrachloride
	chlorinated solvents
	DDT/DDE
	dioxins / TCDD
	pesticides
	phenoxyacetic herbicides
	tobacco smoke (active smoking)

Source: ⁴⁰ .

Ionizing Radiation

Ionizing radiation can result from diagnostic medical x-rays; radiation treatment; exposure to atomic bomb explosions; employment in mining (uranium and tin), the military, airlines (as flight crew), or the nuclear industry; or employment as a medical radiation worker.

As Linet and colleagues (2017) note, the medical field has rapidly increased its use of radiation in diagnostic and treatment modalities, which has resulted in a six-fold increase in radiation exposure from medical sources. ⁴¹ They also report that the use of radiation in diagnosis and treatment has increased the risk of leukemia. For instance, the chronic use of low-dose, alpha-particle radiation for radiologic visualization of vascular structures increases the risk of developing AML. ⁴² Additionally, treating ankylosing spondylitis with x-ray radiation leads to a seven-fold increase of certain leukemia subtypes. ⁴¹ As well, treating ankylosing spondylitis patients with radium-224 nearly quadruples the risk of AML. ⁴¹

Elevated leukemia rates were also found among civilian populations exposed to atomic bomb explosions, including the populations in Hiroshima and Nagasaki and the Utah residents living in proximity to the Nevada Test Sites. ⁴³ Additionally, one study found elevated leukemia rates among U.S. military personnel who participated in a 1957 nuclear bomb test. ⁴⁴

Formaldehyde

Formaldehyde is a strong-smelling and colorless gas that is widely used to manufacture building materials and many household products, including glues and adhesives, permanent-press fabrics, paper product coatings, and pressed-wood products, such as plywood, fiberboard, and particleboard. ⁴⁵ It is also used to produce additional chemicals, as an industrial disinfectant, and as a preservative in food, cosmetics, medicines, funeral homes, and medical labs. ⁴⁵

Environmental health researchers have discovered the leukemia risk is higher for workers in occupations with high formaldehyde exposure, such as pathologists, embalmers, manufacturing, and anatomists. For instance, manufacturing workers who experienced peak formaldehyde exposure have a higher risk of developing myeloid leukemia.^46,47 Also, there is a higher leukemia risk in the embalming industry, particularly for those who performed many embalmings (i.e., over 3,068) or have been in the industry for an extended period (over 34 years). ⁴⁸ In 2012, IARC determined there was adequate evidence to designate formaldehyde as a cause of leukemia, particularly for myeloid leukemia.

1,3-Butadiene

1,3-Butadiene is a hydrocarbon that is produced through petroleum processing. It has a gasoline odor and is a colorless gas at room temperature. It is mainly used to produce synthetic rubber, although is also found in fuel and plastics. People are mainly exposed to it in the following occupational settings: petroleum refining, water treatment, the manufacture of raw components for nylon, fossil fuels, agricultural fungicides, and secondary lead smelting. People can also be exposed to it from automobile exhaust; the ingestion of foods contaminated by plastic or rubber containers; cigarette smoke; and polluted air and water from plastic, rubber, or chemical manufacturing sites. ⁴⁹

Researchers have repeatedly found that workers in 1,3-Butadiene manufacturing have excess mortality due to leukemia. ⁵⁰ Moreover, they have established a dose-response relationship between 1,3-Butadiene exposure and CML and myeloid neoplasms.^51,52 In 2008, IARC concluded there was sufficient evidence to link leukemia carcinogenicity with working in 1,3-Butadiene and Butadiene rubber manufacturing plants.

Benzene

Benzene is an organic volatile compound derived from coal and petroleum sources. This chemical has been key to manufacturing numerous products over the past century, including detergents, pesticides, pharmaceuticals, inks, dyes, paints, leather, shoes, and rubber goods. ⁵³ In more recent decades, it has also been used to produce plastics, resins, insecticides, styrene, latexes, polymers, and benzene hexachloride. ⁵³

In 1982, IARC determined there was enough evidence to link benzene to leukemia, particularly for the AML subtype. ⁵⁴ In subsequent years, researchers demonstrated a dose-response relationship between the toxicant and the cancer.^53,55,56 Moreover, researchers have uncovered that tanker drivers have significantly elevated risks of developing AML.^57,58 As well, some studies have reported increased risks of AML among those residing close to oil refineries and in communities exposed to gasoline vapors or air pollution resulting from traffic pollution.^59,60

Pesticides

Researchers have also linked leukemias to pesticides. Mills and colleagues (2005) found a moderate increased risk of leukemias among farmworkers, which was stronger in highly exposed participants and reached statistical significance when the analyses focused on female farmworkers. ⁶¹

A pesticide of particular interest is diazinon, which is used against mites, ticks, spiders, flying insects, ants, cockroaches, and scorpions and in pet flea collars. ⁵⁰ Beane Freeman and colleagues (2005) found significant links between diazinon exposure and leukemia. ⁶² Moreover, an IARC working group (2017) reported that diazinon was associated with elevated risks for CLL among farmworkers and classified the pesticide as a “probable human carcinogen”. ⁵⁰

Another concerning pesticide is malathion, which is one of the oldest and most used organophosphate pesticides. It is used on grain storage facilities, gardens, outdoor residential areas, ornamental nursery stock, roadways, building perimeters, pastures and rangeland, food and feed crops, and regional pest eradication programs. ⁶³ It is used to manage numerous organisms, including hornets, wasps, aphids, ants, flies, fruit flies, caterpillars, moths, mites, spiders, weevils, and scorpions, as well as head and body lice on humans and ectoparasites of horses, poultry, pigs, cattle, and pets. ⁵⁰ Moreover, in 2017, IARC classified the pesticide as a “probable human carcinogen”. ⁵⁰

Researchers have also tied children's leukemia to parental pesticide exposure (both pre- and post-conception). In a meta-analysis of the literature Wigle, Turner, and Krewski (2009) found a moderately strong association between maternal exposure to pesticides (insecticides and herbicides) and childhood leukemia. ⁶⁴ Similarly, Bailey and colleagues (2014) found a significantly increased risk of AML for children of mothers who were exposed to pesticides. ⁶⁵ Additionally, in a study using birth cohort data from five countries (Australia, Denmark, Israel, Norway, and United Kingdom), Patel and colleagues (2020) found an association between a father's exposure to pesticides (insecticides, herbicides, fungicides) and childhood AML. ⁶⁶ Lastly, Monge and colleagues (2007) found evidence suggesting that pesticide exposure to either parent could increase the risk of leukemia in offspring. ⁶⁷ As well, they found that boys had an elevated risk of leukemia when their fathers were exposed to malathion in the year prior to conception.

Government Coverage of Toxicants Linked to Leukemia

The leukemia home webpages for Cancer Australia, NIH, and NHS describe what leukemia consists of and provide links to additional information. For example, the Cancer Australia website provides links to eight sections: “Statistics,” “Risk Factors,” “Symptoms,” “Diagnosis,” “Treatment,” “Finding Support,” “Clinical Trials,” and “Health Professionals,” with the latter providing clinical practice guidelines for each of the four leukemia subtypes. ⁶⁸

My analysis found all three websites obscure, in several ways, the toxicants associated with leukemia. First, all three sites ignored toxicants on every page except the pages that discuss potential risk factors. While the “Risk factor” pages are where it would be most pertinent to provide such information, a case could be made for also including the information on other pages. For example, the pages discussing what leukemia consists of could discuss how environmental pollution can contribute to the development of the disease. However, this is not how any agency presented the disease. Rather, they consistently presented leukemia as a collection of blood-forming cells in the bone marrow that are growing in an uncontrolled fashion. This strictly biomedical framing fails to mention how that uncontrolled growth can be significantly mediated by exposure to toxicants.

A case can also be made for including toxicant information on the “Treatments” page. While such pages are expected to list pharmaceutical, chemotherapy, radiotherapy, and other medical interventions, they could also mention the importance of remediating the individual's living environments (including home, work, and recreational) to ensure that patients are not being exposed to toxicants that could undermine their recovery or lead to relapse.

Regarding the “Risk Factor” webpages, although environmental health researchers have identified 18 toxicants or toxicant classes that are substantively linked to leukemia, the health agencies failed to mention most of them. Table 3 shows the NIH website only mentioned radiation (radiation therapy and exposure to high levels of radiation) and Agent Orange, while the United Kingdom's NHS only listed smoking, benzene, and “some pesticides and herbicides.” The Cancer Australia website offered slightly better coverage. Not only did it mention radiation, smoking, and benzene, it also listed Agent Orange and “some pesticides.” However, even that result is poor as they failed to identify specific pesticides of concern or list the 13 other toxicants/classes substantially linked to leukemia.

Table 3.

Coverage of Toxicant Information on “Risk Factor” Webpages.

Subtype	Reported in Enviro. Health Literature	U.S. NIH	U.K. NHS	Cancer Australia
ALL	radiation therapy	radiation therapy
		chemotherapy	previous chemotherapy to treat another type of cancer	exposure to certain chemicals, including chemotherapy
	high levels of radiation	exposure to high levels of radiation		exposure to high levels of radiation
			smokers
	pesticides
				exposure to certain chemicals, including the solvent benzene
AML	benzene		exposure to benzene	exposure to certain chemicals, including the solvent benzene
	smoking		smoking	smoking
	previous chemotherapy		previous chemotherapy
	high levels of radiation		exposure to high levels of radiation	exposure to high levels of radiation
	radiation therapy		previous radiotherapy
	formaldehyde
	radiation therapy
CLL	pesticides		Exposure to certain chemicals, which could include pesticides and herbicides	exposure to certain chemicals, including pesticides
	Agent Orange	Agent Orange		exposure to certain chemicals, including Agent Orange
	1,3-Butadiene
	Diazinon		Certain hair dyes may increase the risk of developing CLL
CML	high levels of radiation	Exposure to high-dose radiation	Radiation	High levels of radiation
	radiation therapy
	formaldehyde
	smoking
	benzene
	1,3-Butadiene

Sources: ^41,69–79.

I also tracked the website's coverage of the five toxicants with “strong” evidence (formaldehyde, ethylene oxide, radiation, benzene, and 1,3-Butadiene). All three sites failed to mention 1,3-Butadiene, formaldehyde, and ethylene oxide. Moreover, while the Cancer Australia and NHS sites mentioned benzene, the NIH site did not. The only toxicant listed on all three sites was radiation.

The websites also failed to inform readers about how they could be exposed to toxicants of concern. For instance, the sites failed to identify the sources of benzene, which include: tobacco smoke, automobile exhaust, industrial emissions, auto service stations, hazardous waste sites, and industrial sites that make or use benzene, as well as vapors from products that contain benzene, such as glues, paints, furniture wax, and detergents. ⁸⁰ Another example was radiation as all three sites poorly addressed sources of radiation exposure. While the term “radiation therapy” suggests there are medical interventions that rely on radiation, they do not specify what those interventions are, nor that people can also be exposed to radiation from diagnostic procedures. Nor did they mention non-medical sources of radiation therapy, such as working in the nuclear industry, in mining, as medical radiation workers, or as airline flight attendants. Providing information about sources of exposure would enable workers and communities to work toward reducing, if not eliminating, their exposures.

Emphasizing a Reductionist Framing

Even when toxicants are mentioned, the environmental causation perspective can be downplayed by the surrounding context. Brown and colleagues (2001) found that the environmental causation perspective can be delegitimized by an article's focusing on other causal factors, such as genes, medical treatments, and lifestyle factors (such as smoking). ¹¹ In the present analysis, I found that while the three health agencies had little to say about lifestyle factors, they all consistently pushed a genetic framing of leukemia.

One way they did so was by attributing the manifestation of disease to genetic changes. Examples of this are to be found in the initial statements the NIH and NHS made in their respective “What Causes ALL” sections. The NIH site states “ALL happens when there are changes in the genetic material (DNA) in bone marrow cells. The cause of these genetic changes is unknown.” Similarly, the NHS site attributed ALL to “a genetic change (mutation) in the stem cells that causes immature white blood cells to be released into the bloodstream.” These statements are deficient because they suggest genetic changes are occurring in an environmental vacuum and fail to indicate how toxicant exposures could be leading to said mutations.

Another way to emphasize a genetic frame is by listing genetic disorders as a risk factor for leukemia. This was observed in the ALL information provided by all three agencies. All three listed Down's syndrome as a risk factor, with the Australian site also listing Klinefelter syndrome, Fanconi anaemia, Bloom syndrome, ataxia-telangiectasia, and neurofibromatosis. Regarding AML, genetic disorders were listed on the British and Australian sites, with the former listing Down's syndrome as a risk factor and the latter listing that and nine other genetic syndromes, including trisomy 8 and Bloom syndrome. While leukemia may well be linked to these genetic syndromes, the failure to discuss the role of environmental context is at odds with cutting-edge epigenetics research, which understands how disease is mediated by both genes and environmental context. ⁸¹

A third way to emphasize a genetic frame is to suggest the condition runs in families. While this issue was not present on the NHS site, it was present on the NIH site, which listed “Family history of CLL and other blood and bone marrow diseases” as a risk factor for CLL. The issue was more prominently featured on the Cancer Australia website, which lists “having an identical twin with ALL,” “having an identical twin or close relative with AML,” and “having a close relative with Chronic Lymphoid Leukemia” as risk factors for the three respective subtypes. Although familial predispositions may exist, these statements fail to convey that such predispositions can be traced to having lived in similar environmental contexts and, thus, having faced similar toxicant exposures. Regarding twins, it should be noted they shared the same womb, which, as was previously explained, can be a source of significant toxicant exposure. ²¹

The fixation on a genetic frame is problematic because it obscures the contributing role of environmental factors. Moreover, Sandra Steingraber (2009) argues a fixation on genes is particularly troublesome because genes are the one part of the equation that cannot be altered. ⁴

The Social Costs of Obscuring Environmental Causation

The health agencies’ deficient toxicants coverage obscures the significant relationship between environmental pollution and disease, which has several consequences. First, masking the relationship perpetuates a reductionist understanding of disease, where people attribute diseases to faulty genes and/or lifestyle choices, rather than the environmental pollution that the bodies were exposed to or the political economies that enable and encourage pollution.

In turn, reductionist disease framings impact social responses to medical problems. Doctors and patients who hold reductionist dominant framings will focus on symptom suppression, which, in twenty-first-century industrialized countries, will invariably consist of pharmaceutical treatments. While this approach might help eliminate the bodily manifestation of disease, it ignores the environmental pollution that contributes to disease, which decreases the likelihood such problems will get addressed. This condemns many to being exposed to disease-causing pollution. Importantly, this environmental injustice is disproportionately shouldered by low-income communities and communities of color, due to discriminatory practices that make them more likely to reside, work, and play in polluted environments.^{22,23,82–84}

Reductionist disease frames also have social policy implications. If citizens understand that pollution contributes to disease, they will be more inclined to pressure politicians to order a clean-up and to prevent reoccurrences by enacting punitive regulations and strong enforcement. ⁸⁵ Conversely, publics that adhere to a reductionist frame are less likely to mobilize against environmental pollution.

These problems also engender tremendous societal costs. The failure to address the upstream sources of disease leads to unnecessary disease incidence and increases societal health expenditures. This point is illustrated by examining the case of AML (which accounts for 20–25% of new leukemia cases). In 2010, the U.S. treatment costs for AML were estimated at $191 million and productivity losses were estimated at $60 million. ⁸⁶ Preventing as few as 10 percent of such cases would save significant money, which could be reinvested in other disease prevention programs.

On the other hand, some entities benefit from obscuring toxicant information. As McGoey (2012) emphasizes, ignorance is more than a void to be filled, as it is also a resource that those in power can utilize strategically. ⁸⁷ In this instance, perpetuating ignorance about toxicants shields polluting industries and politicians from public scorn, as well as legal and financial liability. Additionally, maintaining the public's ignorance about toxicant harm further benefits industry by making it easier for them to successfully deny and create uncertainty about harms associated with their products.^6,8,88 It would be harder to succeed in these endeavors if public health agencies were adequately informing the public about toxicant harms. Also benefiting from the situation are pharmaceutical manufacturers and the medical profession, which profit from a steady, if not increasing, production of new patients.

Accounting for the Obscuring of Environmental Causation

To account for the agencies’ deficient coverage I use a synthetic framework that draws on Brown and colleagues’ (2001) “dominant epidemiological paradigm” (DEP) concept and insights from the political ecology of health. ¹¹

In their analysis of print media's coverage of breast cancer, Brown and colleagues (2001) attributed the lack of toxicant information to the DEP, which they define as the “general belief system about the existence and causes of disease” (11, p. 749). As Barbara Ley (2009) eloquently describes for breast cancer, the DEP in Western democracies is reductionist in that it situates the source of disease in genes and lifestyle choices, while de-emphasizing the role of environmental context. ²⁵

Although a reductionist DEP helps explain the dominant institutions’ tendency to disseminate information that ignores or downplays the role of environmental pollution, a deeper analysis calls for identifying factors that shape the DEP. Here too Brown and colleagues’ (2001) work is useful as they identify four influential groups: (a) the science sector (including the teaching enterprise, professional leaders, the “literature,” journal editors, conferences, and professional organizations); (b) government (including research funding sources, government agencies, and politicians); (c) the private sector (including think tanks, activists and social movements, media, disease groups, and medical philanthropies); and (d) patients, who reinforce the DEP by accepting its way of conceptualizing and treating disease or challenge it by making appeals to science, government, or the private sector. ¹¹

One limitation with the DEP framework is that it underanalyzes the political economy's role. To address this limitation, I draw on insights from political ecologists of health. In analyzing the circulation of health and medical knowledge, Jackson and Neely (2015) emphasize the need to start from the premise that all knowledge is situated and thus partial. ⁸⁹ Knowledge producers are informed by their experiences and standpoint, which mediates what aspect of health and disease they study and how they study it. While the sum of their experiences enables them to see and understand certain aspects of health, it also blinds them to other aspects and perspectives, thereby producing incomplete knowledge. From this perspective, one should expect to find important gaps in the disease information promulgated by dominant institutions.

Moreover, Jackson and Neely (2015) emphasize that such knowledge gaps are not randomly produced, but rather are heavily shaped by power. ⁸⁹ In other words, those with power will significantly shape what knowledge gets produced and circulated. Invariably, this means the health information that is disseminated will tend to be what is most beneficial to the dominant class. This underscores the necessity to situate the circulation of deficient disease information within its larger political economy.

An important step in analyzing the political economy is utilizing an adequate conception of the state. The dominant view in academia is to conceptualize Western governments as being pluralist in nature, where various interest groups (including activist groups, industries, professional associations, and unions) vie against each other to influence government policy and action, which prevents any one group from dominating the others. ⁹⁰ However, a conflict theory approach argues such conceptions are ill-suited for modern Western democracies, where it is commonly understood capitalists exert much more influence than other groups. ⁹⁰ From this perspective, one should expect to see government actions tilt toward protecting industry interests. This is manifest in the U.S. government's regulation of toxicants, which assumes chemicals are innocent until proven guilty, allows chemicals on the marketplace without adequate safety testing, and hands out weak fines that fail to deter polluting activities.^4,91

From this perspective, the health agencies’ obscuring of environmental causation can be seen as another instance of governments protecting industry interests. Conversely, if they adequately covered toxicants, doing so would highlight how toxicant manufacturers and users are contributing to disease, which would likely expose these “disease manufacturers” ⁹² to public scorn, as well as legal and financial liability. Additionally, it could prompt the public to pressure politicians to clean up the problem and strengthen regulations and enforcement pertaining to the production, use, and disposal of toxicants, if not ban certain toxicants altogether.

Conclusion

This article's overarching focus was to illuminate how government health agencies cover the environmental causation of disease. Toward that end, I analyzed the leukemia information offered by Cancer Australia, the U.S. NIH, and the U.K.'s NHS. The study revealed that all three health agencies systematically obscure toxicants’ contribution to disease by failing to identify most toxicants that environmental health researchers have substantively linked to leukemia and by emphasizing a biomedical framing of the disease.

This study suggests that, like other dominant institutions, government health agencies are actively obscuring the disease-causing role of toxicants. This perpetuates the general public's ignorance about toxicant harmfulness and condemns many, particularly among the poor and communities of color, to develop preventable cancer.

One limitation with this study is that it only examined the information provided about leukemia. Adding other diseases to the analysis (such as asthma, diabetes, or other cancers) might reveal that coverage of environmental causation differs significantly from one disease to the next, which would be worth exploring. Another limitation is that the study examined the health agencies independent of the other dominant institutions in their countries. Studying other dominant institutions (such as the medical profession) might reveal variation that would warrant further exploration. Research is also needed to better understand the process through which public health agencies assemble medical information they promulgate to the public. This includes identifying who is responsible for assembling that information, how they get appointed to those positions, and the social processes that guide their information selection, as well as the frameworks, institutional affiliations, and other social considerations that discourage them from communicating current environmental health research.

Although dominant institutions obscure the environmental causation frame, it needs to be said that many are working to change the situation. Besides environmental health, there are scientific organizations (such as the Silent Spring Institute and the Collaborative on Health & the Environment) that work to educate the public about this issue. ⁹³ Additionally, environmental justice activists are publicizing the links between environmental pollution and disease in local communities, as well as organizing communities to eliminate those problems.^25,93–95 In the medical field, individual health care practitioners, such as functional medicine doctors, have pursued environmental health training and have incorporated the knowledge into their clinical practice. Moreover, some practitioners with an online following (such as Dr. Andrew Weil) have integrated toxicant information into their website content. While these efforts are important, their capacity to bring about change is neutralized by the fact that public health agencies and other dominant institutions continue to systematically obscure the role of toxicants.

Author Biography

Manuel Vallée, Ph.D., is a Senior Lecturer in the Sociology and Criminology Department at the University of Auckland, where he teaches Sociology of Health, Illness, and Medicine; Environmental Sociology; Sociology of Science & Technology; and Global Issues and Sustainable Futures. He is interested in the intersection between environmental pollution and health, and one way this interest has manifested itself is by studying how this relationship is obscured by the medical information that is disseminated by dominant institutions, such as mass media, medical associations, and government health agencies. He has written several articles on the matter, including ones that analyzed the production of knowledge about Attention Deficit Hyperactivity Disorder and depression. He is also interested in the social production of pesticide use, with a particular focus on the way this practice is shaped by culture and political economy. In the past, he has written about urban aerial pesticide spraying operations, including an article that appeared in Environmental Sociology, another that appeared in the volume Resilience, Environmental Justice and the City, and his recent book Urban Aerial Pesticide Spraying Campaigns (2022). He is now studying citizen movements dedicated to curbing pesticide use.