ATSDR released the draft of the Phase 2 study in December 1999, 26 months after the testing, stating this goal: “a follow-up study to evaluate residual respiratory, dermatological, ocular and neurological effects in community members exposed acutely to chlorine” and to evaluate for “an increased prevalence” of these symptoms.1
“Study participants completed a questionnaire, had blood drawn to measure IgE levels” to control for allergies, “underwent skin and eye examination by a physician, and had breathing tests (pulmonary function tests and methacholine challenge test) administered.” Finally, “the exposed and control groups were compared with regard to various self-reported symptoms.”
Because of budget constraints, ATSDR only sought 150 participants out of the 682 people from the Phase 1 survey. Because of distrust of ATSDR, it seemed, only 121 people participated (within the boundary constraints of ATSDR) in the exposed group, with 99 participants in a control group.
On its face, the ATSDR cautiously confirmed that many victims of the spill suffered chronic eye, skin and respiratory symptoms—and possibly other effects—18 months after the spill.
In dermatological examinations, more than 20% of spill victims reported a persistent or intermittent rash, or rash longer than two months, a rate three to five times higher than the control group. One third had a current rash, compared to one fifth of the control.
Upon examination, rashes on exposed participants were most prevalent on the face and arms. The study noted, “These rashes were described mostly as dry skin, papules, flat macules with color changes, and keratinization…. These descriptions do not seem to be what would be expected from chlorine exposure (chloracne)….” (Emphasis added.) “However, the examining physicians did indicate that the skin abnormality may be due to chlorine exposure for 11 exposed [of 41 exposed people with current rashes] and only 1 control participant, so possibly the rashes seen in the exposed participants are the long term sequelae of an acute exposure to chlorine.”
Notably, the report didn’t consider exposure to other chemicals in the spill as a possible confounder to explain the bulk of the chronic rashes. The report also refrained from recognizing a new type of chronic skin sequelae from chlorine exposure.
In eye examinations, exposed subjects had greater eye problems in 9 of 12 categories, with two symptoms “most strongly associated with exposure” by examining doctors: eyelid margin inflammation (exposed 9.9% / control 3.0%) and meibomian gland inflammation (exposed 8.3% / control 1.0%).
In general, “Of the eye or skin abnormalities noted, the examining physician was more likely to think they were possibly due to chlorine exposure in the exposed than the control subjects,” the report concluded. Physicians recommended that “26.4% of the exposed and 11.1% of the control subjects be referred for follow-up care.”
Not only were the results significant, they were somewhat groundbreaking, though the study refrained from emphasizing this.
“There is not much previous research on the long term effects of an acute chlorine exposure on the skin and eyes. Based on these findings, more study may be warranted.”
But ophthalmologist Dr. Rick Neumeister, who treated about 60 Alberton victims, wrote of the ATSDR Phase 2 study: “It’s findings represent an important development in the field of ocular medicine in that it appears to be the first methodical study to evaluate the long-term eye injuries in a population of persons” exposed to a single exposure of chlorine.13 Neumeister’s Alberton case studies also documented chronic eye injury.7
Overall, the pulmonary function tests (PFT) gave less conclusive results. Concerning subgroups, the study found that “statistically significant or nearly significant differences between exposed and control participants” were noted for females, subjects without preexisting respiratory symptoms, and those without preexisting asthma. These differences suggested “possible persistent obstructive lung changes due to chlorine exposure.” Other subgroups had less conclusive results or showed worse results in the control group.1
“In general, these findings are not what was expected, in that it would have been predicted that subjects with preexisting respiratory abnormalities or a history of cigarette smoking would be more likely to have lasting effects of chlorine exposure reflected particularly in decreased FEV1. There are several explanations for the findings that those without respiratory abnormalities and non-smokers showed the greatest effect of exposure when compared with control participants. The controls may have had poorer preexisting respiratory health than the exposed group(also suggested by the increased prevalence of preexisting asthma in control compared to exposed participants)….” (Emphasis added. But this was a different subgroup.) “It is also possible…that current or former smoking so overwhelms the respiratory system that the effects of the exposure can only be seen in the non-smokers. Another possibility is that the levels of exposure to chlorine actually experienced by the exposed group are quite variable…. Given the difficulties in modeling the chlorine exposure…it is possible that some individuals without much chlorine exposure are included in the exposed group.” (Emphasis added.)
With the methacholine challenge test (using an inhaled drug similar to a histamine), only about two-thirds of the exposed participants and three-fourths of the control participants completed the testing (a significant rate difference in itself): “Of these, about 36% of the exposed and 27% of the control subjects were defined as having abnormal methacholine challenge testing results.” Exposure was associated with an abnormal test result among those without preexisting respiratory symptoms, those with preexisting asthma, and those who never smoked. “The most interesting result is the nearly three times increased risk of abnormal methacholine challenge test result among exposed versus control participants without preexisting respiratory symptoms.” (Emphasis added. Suggesting they had become sensitized.)
Not only did a higher percentage of exposed participants have abnormal methacholine challenge test results, because of a variety of precautionary health concerns (including respiratory), a lower percentage of exposed were able to take the methacholine challenge test. Potentially, then, respiratory sensitivity among the exposed group was even greater than the methacholine test suggested.
Additionally, almost all self-reported symptoms were more prevalent in the exposed group. In addition to a greater prevalence and frequency of skin, eye and respiratory problems, the exposed group reported significantly more gastrointestinal symptoms (diarrhea, vomiting, burning throat and chest pain), unusual fatigue and drowsiness, aching muscles and joints, colds and sinus and respiratory infections.1
Of self-reported respiratory symptoms, the report said, “although more control than exposed participants reported ‘Doctor diagnosed’ asthma and other lung disease, more exposed than control participants reported ever having experienced various respiratory symptoms, having experienced the various respiratory symptoms only after the accident, and having various respiratory symptoms worsen after the accident, if they had also been present before.” The exposed group had more symptoms of wheezing/whistling, chest tightness, shortness of breath with non-strenuous activity, shortness of breath after strenuous activity, being woken at night by shortness of breath or coughing, cough or phlegm in the morning, and shortness of breath when exposed to dust/pets/feathers. While more in the control group had ever had incidence of asthma attacks (20% vs. 13%), slightly more of the exposed group had ever taken medications for asthma, reported regular trouble breathing, and breathing that was never quite right.
The study offered a self-critical caveat regarding self-reported symptoms:
“Making any conclusions about this is difficult, however, because the way in which the questions were asked – ‘Since the train accident, are you having ___ more than usual?’ – provides a very strong point of reference for exposed participants but not for control participants…. Questions framed this way may bias the exposed group toward over-reporting or better-remembering of their health problems compared to the control group. This is suggested by a higher prevalence of every single self-reported health problem among the exposed compared to the control participants.” (Not necessarily, since this study had assumptions about expected health effects from the spill.) As for self-reported respiratory symptoms, “it is, perhaps, notable that this pattern did not hold true for the question about swollen feet,” (meant to assess reporting bias) “which was located in the midst of the questions about respiratory symptoms. This may argue against over-reporting. However, the placement of this question makes its utility somewhat uncertain.”
In sum: ATSDR needed to read their own critiques to help them better design their own studies.
As mentioned above, self-reports on doctors’ diagnoses for respiratory conditions were greater in the control group: lung disease other than chronic bronchitis/emphysema/COPD (exposed 14.1% / control 21.2%), asthma (exposed 10.7% / control 23.2%).
Why night there be significantly more respiratory diagnoses for the control group (despite the pulmonary function tests showing little difference overall between the groups)? Despite warnings from Lucinda Hodges, ATSDR had chosen the nearby towns of Piltzville, West Riverside and Milltown, just east of Missoula, as sources for the control group, all towns close to a major lumber mill, downwind of the Frenchtown mill and the Missoula valley, and prone to polluted air inversions.
Demographics showed that more of the exposed participants were over 35 years of age (78.6% / 65.6%); the exposed had less education (4-year college grad or higher: 15.7% / 43.4%); exposed had lower family incomes (above $20,000: 69.4% / 77.8%); more exposed people smoked (never: 38.8% / 54.6%; current: 31.4% / 17.2%; passive smoke exposure: 47.9% / 25.3%); and more exposed had greater occupational dust exposure (43.0% / 35.4%) and occupational VOC exposure (57.0% / 54.6%). From this cross-section, at least, the Alberton population emerged as less educated, poorer and older than the controls, with greater vulnerability to lung ailments from work and smoking exposure (but likely a cleaner local airshed for particulates).1
Despite the exposed participants being older, having a greater history of smoking and occupational dust and VOC exposure, and the fact of their derailment exposure, fewer had doctor diagnoses for some lung disease and asthma, and had about the same rate of diagnoses for other lung diseases and allergies. And in PFT tests, the exposed group only showed significantly worse function in certain subgroups, such as among women, non-smoking participants, and those without preexisting respiratory symptoms.
Yet, the exposed group self-reported a much higher rate of respiratory problems.
ATSDR considered the matter:
“The control group reported more doctor diagnosed lung disease other than chronic bronchitis/emphysema/COPD and more doctor diagnosed asthma…. Inadvertent recruitment of a control group with poorer respiratory health than expected may have occurred…. At the same time, as stated earlier in the Report, the control group exhibited a higher socioeconomic status than the exposed group. Therefore, the control participants might have a more comprehensive medical insurance which might result in a more realistic knowledge of their underlying respiratory disease.”
The Bonner mill near West Riverside and Piltsville boosted the local economic status—along with company health insurance, the control group could better afford doctor visits.
That state and local health officials thought communities with bad airsheds would make good controls was dubious. Many sensitized Alberton victims complained of Missoula’s air, before and after the spill.
Tellingly, though more exposed felt “more sensitive to chemicals than most people” (43.8% / 24.2%), and more exposed felt chemically sensitive after the spill (43.8% / 23.2%), even the control percentages seemed fairly high. When asked how concerned they were that something in their neighborhood environment may be harming their health (in the fall of 1997), the exposed group expressed less concern than the control group:
Not at all 46.3% / 40.4%
A little 28.9% / 33.3%
Very 24.8% / 25.3%
Not only did the control communities have well-known air pollution concerns, but they lived near the Milltown Dam along the Clark Fork River, a Superfund repository for toxic mining sediments that had contaminated many wells. Everybody knew this, including Alberton victims, but ATSDR did not heed their protestations.
The study also failed to note that, in addition to the exposed group having had less medical insurance and care before the spill, many Alberton victims had to deal with financial and insurance problems after the spill that competed with medical care dollars, as well as deal with some doctors skeptical of chemical-induced asthma or sensitivity.
Regardless of these inequality issues, though more of the control group self-reported ever having an asthma attack as did the exposed group (20.2% / 13.2%), many more exposed had their first asthma attack after the spill (5.8% / 1.0%) and many more exposed with pre-existing asthma had asthma symptoms worsen after the spill (5.0% / 1.0%). Just as telling, though only slightly more of the exposed group had ever taken medication for asthma (22.3% / 21.2%), many more exposed had taken medication for asthma for the first time only after the spill (12.4% / 2.0%). The exposed group, which generally reported higher rates of ever having problems breathing, was eleven times more likely to report the first onset of breathing problems occurring after the spill. The methacholine challenge results for exposed participants also suggested that victims suffered respiratory sensitivity from the exposure.
The inequality caveats and the parsing of the data suggested a much greater respiratory impact of the spill on the exposed group than the study recognized.
ATSDR also claimed to study the neurological effects of Alberton’s chlorine exposure, while noting “very limited evidence in the literature for chronic adverse neurological effects following acute chlorine exposure,” citing only Dr. Kilburn’s 1995 study of seven people. (Kilburn’s first study of Alberton victims was published in 1998, and the preliminary draft available in 1997.6,5) “In general, it is not accepted that chlorine is directly neurotoxic.”1
Nevertheless, the study design included ‘neurological methods’ because “concerns and anecdotal reports regarding neurological problems had been received from the community, and ATSDR felt it necessary to address these issues.”
The study found that “a higher percentage of exposed than control subjects answered ‘Yes’ to each of 16 neurological screening questions,” (not isolated as “neurological questions” to tip off the client) “including one question which is supposed to assess response bias.” Developed by Dr. Christer Hogstedt in the 1980’s, the questions had been “validated by Hogstedt in field trials against the results of neurobehavioral test batteries, were initially used for those exposed to solvents, have also been used for those exposed to lead and have been successfully employed by ATSDR in a similar community based study,” Bunker Hill, Idaho.
In all 16 neurological screening questions, exposed participants were two to four times more likely to answer ‘yes’ to questions about memory problems, difficulty concentrating and understanding, confusion, dizziness, irritability, depression, insomnia, loss of interest in sex, heart palpitations, chest pain, excess sweating, and headaches. The exposed group also answered more frequently the response bias question about “any problems with buttoning” (9.1% / 1.0).
The exposed group answered ‘yes’ to six or more positive neurological screening questions more often than the control (51.2% / 13.1%).
“It is unclear how the results of this screening questionnaire should be interpreted for this study,” the report said. Although the exposed group had overwhelmingly reported more neurological symptoms than the control group, they had also reported more difficulty with buttoning buttons, which was supposed to reveal response bias. Notably, however, the percentage of exposed answering positive to the button question (9.1%) was a fraction of the positive range for all other questions (20.7 / 68.6%). Also, the test design assumed that fine motor skills were not affected by the exposure.
“There may be over-reporting going on…or these results may be an actual indication of neuropsychiatric problems in the exposed participants. Given the lower socioeconomic status of exposed participants compared to control participants and the stress on exposed participants due to the derailment and its after-effects, an increased prevalence of neuropsychiatric illness in the exposed subjects before and/or after the derailment would not be surprising. Other possible and unmeasured causes of neuropsychiatric illness, which might explain some of the findings, include other exposures….” (Emphasis added.)
However, the ATSDR study never seriously considered spill-related exposures other than to chlorine:
“The questionnaire’s use in this study was primarily to address residents’ concerns about neurological symptoms, as it has not been shown that chlorine is neurotoxic, nor has the presence of any other chemicals besides chlorine from the derailment been documented off-site.”
Given ATSDR’s foregone conclusions about spill-related exposures and the effects of chlorine, did ATSDR study Alberton victims’ concerns of neurological damage or merely patronize them?
As with other self-reported symptoms, the report reiterated that interpretation of the neurological questionnaire was made difficult due to the possibility of bias in relation to an important event—the spill. “It is not surprising that the prevalence of nearly every symptom in our [self-reported] questionnaire was higher among exposed than control subjects after the derailment, and nearly every symptom already present worsened after the derailment in the exposed participants. This may be due to actual health differences among exposed and control groups, or it may be due to recall bias….”
Unlike with other self-reported symptoms, ATSDR failed to have participants evaluate whether any neurological-related symptoms had first appeared or worsened after the spill exposure, which would have aided in evaluation of the data.
“Considering the known difficulties in the use of self-reported symptoms to compare exposed and control groups, more objective measures of the long term effects of an acute exposure to chlorine were collected: the physician exam, pulmonary function tests, and the methacholine challenge test.”
By their own words, ATSDR never seriously considered symptoms other than classical chlorine symptoms, or presumably “more objective measures” would have been inculcated in the study design to allow more objective conclusions.
An ATSDR doctor would later confirm that the neurological ‘study’ held little significance—by design.
The study also included background interview questions from which no interpretive data was culled. From this, the report only noted that “anecdotal reports of continuing health problems in the affected community have been received by ATSDR from a number of sources.”1
In the questionnaire, victims were asked:
“Do you remember smelling chlorine – a smell like that of liquid laundry bleach – on the morning of April 11, 1996, the day of the spill?” and, “Do you remember smelling chlorine – a smell like that of liquid laundry bleach – at the accident site?” No question asked about any other smell, despite many ‘anecdotal reports’ of smelling a pesticide-like smell and other smells.
The report reiterated that ATSDR’s Health Consultation—a document review of the EPA START report and of the clinical examinations of people immediately after the derailment—had concluded that while chlorine had migrated off site, “available data did not indicate that other chemicals spilled in the accident or any of their reaction products (such as chlorinated phenol compounds produced from a chemical reaction between chlorine and potassium cresylate) migrated off-site.”
A few chemical sensitivity questions were included as well, such as: “Do you feel you are more sensitive to chemicals than most people?” For those in the exposed group who reported becoming sensitive to chemicals, they were asked how soon sensitivity happened after the spill; “In what way does a chemical make you feel bad?”; “What chemical or chemicals make you feel bad?”; and “What about chlorine? Do you feel you are extra sensitive to things that may contain chlorine like liquid laundry bleach, automatic dishwasher detergent, swimming pool water, and tap water?”
Without comment, data on answers to these questions was not summarized by ATSDR. In other words, ATSDR chose not to study chemical sensitivity from the spill—despite that sensitivity was one of the major general complaints victims had reported directly to ATSDR. ATSDR also failed to ask if people felt their sensitivity was triggered by their home or the Alberton area environment.
Incidentally, in their literature review, ATSDR noted “there have been reports of individuals with one acute exposure to chlorine who appear to be suffering chronic respiratory effects from the exposure. Schonhofer et al [1996] followed-up three exposed individuals, and noted bronchial hyperresponsiveness and reactive airways dysfunction syndrome more than 2.5 years post exposure. Schwartz et al [1990]…noted airway hyperreactivity in 5 of 13 individuals, 12 years after exposure, that appeared to be directly related to the degree of airflow obstruction and air trapping observed immediately after exposure, and hence may be related to exposure. Boulet [1998] reported on two cases of exposed individuals, one exposed to hydrochloric acid and the other to a bleaching agent which contained chlorine, with bronchial hyperresponsiveness present one and six years after exposure, respectively. The presence of mild preexisting asthma in the first case may have exacerbated the effects of exposure.”
Other research, the report concluded, including one post-Alberton spill study, “does not suggest chronic effects of chlorine exposure,” though three earlier studies “did not assess bronchial hyperresponsiveness.”
But as with chemical sensitivity, ATSDR chose not to study bronchial hyperresponsiveness and reactive airways dysfunction syndrome with the Alberton victims, despite the fact that, by ATSDR’s own review, there was inconclusiveness of results in the literature and scarcity of data. Additionally, Dr. Cynthia Lewis-Younger, following her clinical evaluation in 1999 in which she discovered previously undiagnosed cases of RADS in Alberton spill victims, recommended that ATSDR conduct more comprehensive peak flow studies for Alberton to determine the prevalence of RADS. ATSDR did not do this.4
ATSDR had looked opportunity in the face, the kind of opportunity that Dr. Kaye Kilburn focused intently upon, and averted its gaze.
When asked how concerned they were that the chemicals spilled in the train wreck had harmed their health, the exposed group answered:1
Not at all 32.2%
A little 33.9%
Very 33.9%
When asked how concerned they were that the chemicals spilled in the train wreck may harm their health in the future, the exposed group answered with a little more concern:
Not at all 28.1%
A little 30.6 %
Very 40.5 %
The split may give insight into the various divisions within the greater Alberton community concerning the spill and its aftermath. Whereas the questions were vague as to whether any harm to health was ongoing, the answers suggested that two-thirds of the participants felt they had mild to significant chronic health symptoms in the fall of 1997.
Which spill victims did the study follow-up on?
Back in 1997, ATSDR tried to explain to angry residents why only certain people would be tested in Phase 2: ATSDR would adhere to assumptions about exposure, namely that modeling suggested those closest to the spill would have the highest exposure. With the published study, ATSDR admitted they abandoned trying to categorize exposure groups based on air modeling using geography and temporality because of “numerous uncertainties and difficulties in this modeling, as well as uncertainties in individual risks for exposure.” Nevertheless, selection from Phase 1 participants for the Phase 2 study was based on proximity to the derailment, and exposure was assumed to be greatest for participants “residing within about 8 miles downwind,” east of the spill—the simplest model possible.1
“There is a high likelihood that those residents receiving the highest exposure were included in the selection,” the report asserted. Yet, this was deemed a follow-up study, so people not participating in Phase 1—geographically eligible residents like Hodges, Griffin, Robertson, and Ridenour—were not eligible. Also, no effort was made to keep track of the unknown number of people that left the area due to their sensitivity to the area or other reasons. Presumably, some emigrants that had lived within that eight-mile zone may have developed sensitivity great enough to drive them to relocate. The study ignored them, or knowing about them.
Further exclusions: of the 682 people from the Phase 1 Study, “only those persons between the ages of 24 and 65, for whom there was substantial evidence of acute chlorine exposure effect were eligible for enrollment in Phase 2. The purpose of the age limitation was to minimize the affect of age on pulmonary test outcome, and also to avoid performing these tests [methacholine challenge]…on children.” It wasn’t clear why older children and adults to age 24 were excluded.
After these screenings, “available exposed persons included 104 men and 115 women.”1 But of these 219 people, only 132 made appointments, with 121 actually seen—a participation rate of only 55% of those eligible.2
While many ineligible victims had been angry over exclusion, ATSDR now bemoaned a “poor participation rate,” which, predictably, made interpretation of test results more difficult.1
The available control subject pool consisted of 228 people. (Other than screening for age and sex, the comparisons weren’t that similar, as demographic information showed.) Only 44% of the eligible pool participated, 99 people.2 Control participation was typically a problem (though presumably not because of anti-ATSDR bias).
In reality, the cohort of eligible participants was mainly determined by the limited budget, which only allowed for a maximum of 150 exposed and 150 controls. In order to still appear ‘objective,’ eligibility parameters had to be narrowed and shaped in an attempt to identify a potential exposed group that would not exceed 150 people, after factoring in expected participation rates.14
Additionally, ATSDR didn’t follow up on their original survey of 23 first responders, which found 16 reporting health problems within two weeks of the spill.15
Limited participation—by design.
The ATSDR Phase 2 report concluded:1
“The results of this study suggest that an acute exposure to chlorine following a train accident may have had chronic health effects on exposed persons. Various study limitations, including poor participation rates among eligible exposed and control subjects, issues of recall bias in the analysis and interpretation of self-reported symptoms, uncontrolled confounding, and difficulties in exposure assessment, make cautious interpretation of the study results necessary….
“Given the occupational literature and suggestion of effects noted in this study, if a similar situation were to arise, another study of this sort should be attempted. Hopefully, better air monitoring data and less uncertainty about the toxin release and migration would enable a more accurate exposure assessment….
“Follow-up of the children and adolescents who were exposed with an emphasis on monitoring health care utilization should be considered.”
Phase 2 had excluded people under age 24.
Translation:
Mainly because of the way the study was designed by ATSDR, results weren’t strongly conclusive. Maybe next time.
The EPA characterized the study thusly:
“Although a cautious interpretation of the study results is necessary due to various study limitations, the results of a Phase II ATSDR study…suggests that an acute exposure following the train derailment may have had chronic health effects on exposed persons.”12
Chris Weis recalled, “I would have liked to see ATSDR do a more thorough follow up on the cohort of people that were exposed too, but that didn’t happen.”8
Regardless of the study’s self-induced limitations and ATSDR’s cautious interpretations, the medical examination results indicated chronic eye and skin symptoms significantly higher among the spill victims than the control, and suggested chronic lung impairment among certain subsets. Self-reported information indicated a variety of other symptoms among spill victims, including chemical sensitivity, and that one-third of spill victims felt their health had been “very” harmed by the spill—perhaps chronically. A neurological questionnaire suggested “neuropsychiatric illness.” But ATSDR failed to meaningfully study neurological effects or chemical sensitivity resulting from the spill—by design.
While ATSDR failed to study MCS—which they recognized as a legitimate illness—and made only cursory inquiry into neurological complaints, another omission was failure to consider psychological damage from the Alberton spill, to perhaps help address some of the neurological complaints. This was an emerging field at the time.
In 1995, ATSDR began a Psychological Effects Program to address stress-related health concerns. Part of this program included a workshop examining “how to perform neurobehavioral testing to determine if any observed neurological effects are caused by chemical or stress effects on the nervous system.” Panel One, examining the biomedical and psychological effects, “was charged with reviewing and discussing how health care providers can clinically examine an exposed individual to determine if health effects are the result of exposure to neurotoxic chemicals or from stress. They found that careful history-taking is essential to ensure differentiation of exposure to neurotoxic chemicals and/or the development of stress-related health effects.”11
This workshop resulted in ATSDR’s Pamela Tucker, MD, publishing the “Report of the Expert Panel Workshop on the Psychological Responses to Hazardous Substances.”3
Elsewhere, Tucker wrote that since Love Canal in the 1970s, “psychologists, psychiatrists and social scientists have studied the psychological responses in people exposed to hazardous substances….”11
It was crucial to determine the cause of psychological effects, if possible. But ATSDR failed to investigate with Alberton, even after ATSDR’s screening test suggested neurological problems.
Tucker wrote in 2000 that current belief held that most people recovered from the psychological stress of a natural disaster, though some may develop major depression. “There are important differences between psychological effects from actual or perceived exposure to chemicals and those resulting from natural disasters.”10
For one thing, natural disaster sites usually returned to normal over time.
“Life near a hazardous waste site is a more nebulous and uncertain situation,” she wrote, a statement that resonated with Hodges.
Even after clean up, “Environmental contamination…in case of exposure, may result in latent health effects for those people exposed to a hazardous substance….
“Living near a hazardous waste site can breed uncertainty about exposures and subsequent latent health effects and spark social and political turmoil, all of which serve as additional stressors. Also, exposure to neurotoxic chemicals can cause psychological changes, so it is important to rule out exposures before declaring a health problem to be solely psychologically based.”
Irrespective of exposure, living near a perceived hazardous waste site could cause chronic stress because of uncertainty. And that stress could also cause physical symptoms, such as higher blood pressure and changes in immune system function. (The dynamic: exposure could cause physical and psychological affects; physical problems could lead to psychological effects; psychological problems could lead to physical effects; finally, exposure could also cause neurological effects.)
Researchers have found “that a linear relationship existed between the degree of gas exposure and the level of psychological distress….”
But, “The critical factors and underlying causes that result in these types of effects from stress are still not understood,” Tucker concluded.
Weis thought the psychological overlay from the Alberton spill was significant.
“I think it’s huge for this kind of response. Arguably, for the majority of people, the long-term psychological effects are probably more important from a public health point of view. At least as important as some of the pathophysiological effects.”8
Weis left the EPA for the National Institutes of Health in 2010.
Following the 2010 BP oil spill in the Gulf of Mexico, Weis said, “For the first time, following the disaster in the Gulf…we’ve been able to convince the Department of Health & Human Services to spend a significant amount of time and effort in assessing psychological consequences of the disaster. And so, we are in the process of building into the federal response system a major psychological component.
“We did a little bit of that for the Alberton derailment because we brought [ATSDR] up to do some of that,” he claimed. “I think they really didn’t have a very good structure to work around to make the assessment, but they tried.”
Or hardly tried. By 1997, ATSDR was holding workshops “to assist communities with the chronic psychological effects of hazardous substances, when requested by communities.”10 They did none for Alberton, and Hodges wasn’t even aware of such workshops. She was well aware of dismissal of certain health effects as being merely ‘in one’s head.’
But despite ATSDR’s Psychological Effects Program, neither the ATSDR Phase 1 nor 2 studies examined psychological effects of the Alberton spill.
Perception matters. Living in a toxic site, or even a perceived toxic site, produces chronic anxiety and stress, perhaps clinical depression. Suspicions about government assurances may prolong the perception that a site deemed safe remains toxic. With threats real or imagined, residents remain uncertain and anxious about their health, the safety of their home and surrounding environment, and about their relationships with the government, community and neighbors, especially with those not similarly affected. They lose trust and control of their lives. If they have strong connections to a place, they wonder whether any given illness might have connections to local contamination, and they worry about the future of their life there and the lives of their children, feeling torn between whether to leave or stay. Others who aren’t sick might think such worries are ‘all in their head,’ further undermining their concerns.9
And unlike a natural disaster, someone is to blame, and one feels victimized.
The main reason residents were relocated from Love Canal, the impetus for the Superfund law, was due to the psychological impacts of living next to a chemical dump, not proven physical illness per se.
Even after the poison is gone, people need to believe the poison is gone.
Overlaying all of this is the potential for neurophysiological and neuropsychological damage from chemicals.
In sum, ATSDR failed to study Alberton spill victims for MCS, despite having developed a questionnaire for MCS; failed to study for RADS, despite Dr. Lewis-Younger’s recommendations following her clinical evaluation; failed to study neurological injury, despite spill victims’ complaints; and failed to study psychological impacts despite Dr. Tucker’s research and Lewis-Younger’s recommendations.4
References
1-Evaluation of Residual Respiratory and Other Health Effects from a Chlorine Release, Draft of the ATSDR Phase 2 Alberton study for Public Comments, December 1, 1999.
2-ATSDR Public availability session in Alberton, Montana, with Chris Poulet, Frank Bove—Division of Health Studies, Dr. Oleg Muravov—medical epidemiologist, December 8, 1999, RL Scholl audio recording.
3-Pamela Tucker, “Report of the Expert Panel Workshop on the Psychological Responses to Hazardous Substances,” ATSDR, US Dept. of Health & Human Services, 1995. https://www.atsdr.cdc.gov/hec/prhs/psych5ed.pdf
4-Dr. Cynthia Lewis-Younger, “Alberton medical intervention summary—draft,” Rocky Mountain Center for Occupational and Environmental Health, April 14, 2000.
5-Kaye Kilburn, “Persisting neurobehavioral and pulmonary impairment after chlorine exposure,” draft document, January 28, 1997. (ACCEH file)
6-Kaye H. Kilburn, Chemical Brain Injury (Van Nostrand Reinholt: New York, NY, 1998).
7-Dr. Rick Neumeister deposition, October 12, 1999, in Mayo et al v. MRL (CV-98-109-M-DWM) (US District Court, District of Montana, Missoula Division).
8-Chris Weis, RL Scholl interview, 2011.
9-Michael Rivlin, “The Super Stress of Superfund,” The Amicus Journal, Winter 1999.
10-Pamela Tucker, MD, “Scientific Research Continues on the Psychological Responses to Toxic Contamination,” ATSDR, Hazardous Substances and Public Health, Vol. 10, No. 1. Spring 2000.
11-Pamela Tucker, MD, “ATSDR’s Psychological Effects Program Address Stress-Related Health Concerns,” ATSDR, Hazardous Substances and Public Health, Vol. 10, No. 1. Spring 2000.
12-“Preliminary Assessment, Alberton Train Derailment,” Superfund Technical Assessment and Response Team 2 – Region VIII, U.S. EPA, April 11, 2003.
13-Dr. Rick Neumeister letter, August 23, 2002, in Walshes vs. MRL (DV-99-87922) (Montana Fourth Judicial District Court, Missoula County) (#138).
14-ATSDR, “Evaluation of residual respiratory and other health effects from a chlorine release,” Phase 2 Protocol, October 16, 1997.
15-ATSDR, “Results of a Health Survey Taken Among First Responders to the Alberton, Montana, Chlorine Release,” August 7, 1996.
