Public health experts estimate that between 500 and 2,000 people die each year in the United States from carbon monoxide (CO) poisoning. Claims professionals presented with a claim of wrongful death or serious physical injury arising from CO exposure obviously will give such a claim careful attention, assign competent counsel, and set the proper reserves. However, not all CO exposure claims involve massive acute exposure and death or serious physical harm.
Many CO claims, if not the majority, arise from low-level exposures that do not result in loss of consciousness and involve little to no medical treatment. Claims are filed months following the exposure event, usually in clusters, and often involve vague and nonobjective findings such as headache, nausea, dizziness, and fatigue. Medical bills may be less than $500 and wage loss nonexistent. Conventional wisdom often warrants setting low reserves, forgoing the expense of top legal talent, and counting on resolution of the matters for nuisance value at some point down the road.
Imagine the shock when demand packages arrive seeking seven-figure settlements for what plaintiff’s attorneys now describe as objectively provable brain damage with commensurate neurocognitive impairment, neurological deficits, and even cardiac injury. Worse yet, it is soon discovered that these demands are supported by neuropsychological tests and state-of-the-art brain scans, such as functional magnetic resonance imaging (fMRI) or diffusion tensor imaging (DTI), and claim to definitively prove basal ganglia abnormalities, hippocampal atrophy, temporal lobe lesions, white matter ischemic changes, and decreased corpus callosum fiber tracts. Suddenly, the plaintiffs’ low-exposure cases are no longer low-exposure claims for the insured and insurer.
Unfortunately, this scenario is playing out much more often around the country. Even more troubling is that, armed with new literature and new imaging technology, plaintiff’s lawyers are convincing juries that verdicts in excess of $30 million are reasonable. The goal of this article is to acquaint claims professionals with this emerging trend, to explain how these low-exposure cases are prosecuted and why they are extremely dangerous, and, most significantly, to provide strategies for defense and mitigation.
The Dangers of Carbon Monoxide
Carbon monoxide gas is the highly toxic byproduct of the incomplete combustion of any carbon-based fuel. Because it is colorless, odorless, nonirritating, and tasteless, it has been dubbed the “silent killer.” It is widely accepted that, once inhaled, it passes through the air exchanges of the lungs and immediately bonds to hemoglobin, which is the oxygen-carrying compound found in red blood cells. The result is the production of carboxyhemoglobin (COHb), which decreases the capacity of red blood cells to transport and deliver oxygen throughout the body thereby causing hypoxic tissue injury, particularly in the heart and brain.
A more recently advanced theory is that, in addition to hypoxic injury, CO exposure also causes cellular changes that result in inflammation that, in turn, causes neurodegenerative damage and impaired brain function. Especially problematic is the fact that CO’s affinity to bond to hemoglobin is 250 times greater than that of oxygen, meaning that hemoglobin will bond preferentially with CO even when a greater volume of oxygen is available.
Prevalence of Carbon Monoxide Poisoning
The Centers for Disease Control and Prevention (CDC) list carbon monoxide exposure as the leading cause of accidental poisoning in the United States. The CDC reports an average of 500 confirmed deaths each year nationwide, although some experts believe the number of deaths is under-reported and could be as high as 2,000. It has been estimated that an additional 50,000 people seek medical treatment in U.S. emergency departments each year. Exposure has been linked to various sources, including improperly vented car exhaust, clogged chimneys or exhaust flues, and improperly installed or maintained gas burning furnaces, gas and wood-burning stoves, gas-powered generators, gas or charcoal burning grills, and gas stoves and ovens.
Ambient Exposure Levels
Symptoms of CO poisoning vary with concentration, duration, susceptibility and activity at the time of exposure. Acute symptomatology occurs quickly at high levels. Chronic exposures to low levels of CO will manifest, if at all, as a constellation of mild, vague symptoms that persist but build over time. Ambient air levels of CO are measured in parts per million (ppm). At 35 ppm slight headache and dizziness can be expected in six to eight hours. The same symptoms can occur in less than three hours when levels rise to 100 ppm. At 200 ppm headache and diminished judgment are observed in two to three hours. Frontal headache within one to two hours is common at 400 ppm. When levels reach 800 ppm, dizziness, nausea, vomiting and convulsions are seen in 45 minutes. As levels approach 1,600 ppm, all of the above listed symptoms are likely within 20 minutes, with tachycardia and death following should the exposure last two hours. At levels over 12,000 ppm, unconsciousness is likely in just three breaths with death occurring in less than three minutes.
Carboxyhemoglobin Levels
Although awareness of the ambient air levels of CO is important, what ultimately determines the degree of illness and injury is a function of the carboxyhemoglobin (COHb) in a person’s bloodstream measured as a ratio of CO to COHb molecules. Most emergency centers will diagnose CO poisoning when COHb levels reach 12 percent. Generally, no observable effects are seen at levels under 10 percent. Between 10 and 20 percent, dilation of vessels begins. Hyperbaric oxygen treatment is typically initiated at 25 percent. Headache is noticed as levels approach 30 percent with nausea and vomiting commonplace by 50 percent. Above 50 percent, convulsions, asphyxiation, and coma occur. Levels above 70 percent are fatal. The half-life of COHb in the blood averages four hours. Administering pure oxygen can reduce this half life to an hour. Hyperbaric oxygen treatment cuts the half-life to under 25 minutes.
Understanding Liability
In light of the potentially devastating consequences of breathing CO, it is generally understood that any circumstance that introduces this gas to any place where people reside, congregate, or work is the result of miscalculation. Most incidents involve the unknowing juxtaposition of people to a known source or the flawed ventilation of a known source. Often large numbers of people are simultaneously affected, requiring the intervention of first responders along with investigation by local authorities.
Building and plumbing codes are implicated when carbon fuel-burning equipment is improperly installed, maintained, or inspected. Code violations in such instances quickly point liability in the direction of building owners, architects, system designers and installers, facility managers, building associations, landlords, and even equipment manufacturers. OSHA recently lowered its permissible exposure limit (PEL) from 50 to 35 ppm over the course of an eight-hour workday, with a peak level of 200 ppm at any given point. Beyond that, 39 states and many cities have passed legislation mandating the installation of CO detectors. The absence of a working CO detector that would have warned those exposed in such a jurisdiction is arguably negligence per se.
Cases arising out of exposure to high levels of CO causing death or devastating injury will obviously be quickly assessed as “high value” and will be afforded top priority and assigned large reserves. Their course, although unfortunate, is reasonably predictable. What is now becoming apparent is that low-exposure cases may merit the same priority and reserves as well.
Low-Exposure Verdicts and Settlements
Concern for the jeopardy imposed by low CO exposure is more than a function of the plaintiff’s bar pushing the envelope on what is fair compensation; it is a function of juries validating them and more. In 2010, a group of 23 Baltimore workers exposed for a short time to moderate levels of CO at a restaurant adjacent to a boiler room with a leak and no CO detectors were awarded more than $34 million. No plaintiff died, none lost consciousness, most did not go to the hospital, and those who did were treated and released within hours. The highest documented COHb level was 27 percent, and no others exceeded 15.7 percent. To put these numbers in perspective, the average COHb level for a two-packs-per-day smoker is over 10 percent. The average for a person stuck in a traffic jam on a summer day is very close to 15 percent.
In 2013, a 20-year-old student in physical therapy school in Wyoming was awarded $28.5 million following a furnace leak in her apartment. As a result of this chronic exposure, the plaintiff alleged headaches, cognitive and memory deficits, sleep disorders, and an inability to complete her degree.
In 2011, a 28-year-old Boston mother and her four-year-old daughter were exposed in their apartment due to a leak from the HVAC unit. Upon arrival at the hospital, the mother’s COHb level was 17 percent dropping to 0.2 percent following treatment. Her daughter’s level was 15.7 percent, which dropped to 0.2 percent. The child had no reported complaints. The mother complained of headache, fatigue, PTSD, and difficulty in caring for her daughter as well as she did before the exposure. For context, pulmonary function testing (PFT) diffusion studies require a patient to inhale a mixture of gases, including 0.3 percent CO. Facing enormous demands, the building owner, facility manager, and HVAC installer settled for over $3 million.
The plaintiff’s bar is now challenging the long-standing belief that, absent exposure sufficient to cause loss of consciousness or similarly severe symptoms, there are no long-term effects from exposure to low levels of CO. Seizing on more recent literature that suggests neurological sequelae may manifest as late as 40 days post exposure in 50 percent of those exposed to low levels, plaintiff’s lawyers eschew traditional defenses based on minor exposures, delays in reporting, or minimal medical treatment. They are enlisting experts to objectively support what was previously relegated to the realm of neuropsychological testing.
Aided by advances in medical imaging—such as quantitative and functional MRIs (qMRI, fMRI), DTI, positron emission tomography (PET), or single photon emission computed tomography (SPECT)—medical imaging experts claim that they can illustrate the patterns of brain injury caused by the pathophysiologic mechanisms of CO poisoning. They now produce films in vivid color purporting to show the exact locations of the brain lesions correlating to the neuropsychological findings and the subjective complaints of the plaintiff. They now testify before jurors with scans claiming to depict atrophy of the hippocampus, decreased fiber density in the corpus callosum, necrosis of the globus pallidus, injury to the basal ganglia, and demyelination of cerebral white matter.
The impact of this evidence can be devastating as jurors are told that they are looking at color images, or “proof positive” depictions, of the actual permanent damage inflicted upon the plaintiff’s brain by CO exposure. Suddenly, the plaintiff’s vague subjective complaints and the psychologist’s confusing terminology become very real, completely objective, and very understandable for jurors who are looking for the simplest choice to make about a complicated medical question. It follows then that jurors do not find it a leap of faith to believe that auditory, vision, and cardiac problems, likewise, are related, and huge verdicts then ensue.
It is therefore imperative that an effective defense to this onslaught begins early. Since it is unlikely that any plaintiff will have scans taken prior to the alleged exposure, complete medical, social, educational, and employment histories must be developed on each plaintiff to construct a pre-exposure baseline.
The plaintiff’s experts will seek to compare the plaintiff’s brain to an otherwise perfect brain. Credible specialists in the field will explain that, for the average adult, no such brain exists. It is unlikely that any active individual reaches adulthood without exposure to many and various prior insults to brain health and function. Birth trauma, infection, anemia, apnea, prior loss of consciousness, or concussion are all potential causes of what the plaintiff’s imaging may show.
Find out about the plaintiff’s social habits. Is there a history of smoking, drug or alcohol abuse? Was the plaintiff an athlete involved in a contact sport with repetitive impacts as in football, soccer, or martial arts? What is the plaintiff’s occupation? Has there been regular exposure to solvents, chemicals, fumes, vapors, or loud noise. Is there a family history of degenerative illnesses such as Multiple Sclerosis, Alzheimer’s, Parkinson’s, depression, anxiety, ADD, ADHD, or bipolar disorder?
School records often contain years of baseline testing and cognitive evaluation that may reveal long-existing problems similar to those now blamed on CO. Thorough searches of social media sites could reveal activities and behaviors that establish other potential causes of abnormal imaging or provide evidence that the plaintiff is not being candid about his alleged injuries. Needless to say, this type of investigation cannot be done quickly.
Much is developing in medical and scientific literature as to exactly what the new imaging is accurately depicting. Many reputable scientists will stop far short of agreeing that this technology is actually documenting what plaintiff’s lawyers say it documents. Selection of the right defense experts will assist in reining in overreaching testimony and set the stage for well-supported Daubert and Frye challenges.
Do not underestimate the steep learning curve on these cases. Retaining counsel with significant experience in CO exposure cases will allow the claims professional to get up to speed quickly on a case’s potential. Counsel with a working understanding of the science relied upon by plaintiffs will likely already know the plaintiff’s counsel and experts and will have immediate access to the best available defense witnesses. Claims professionals and risk managers who align with experienced counsel and understand the science, medicine, and legal issues associated with this emerging trend will be well positioned to react quickly and effectively when these claims present.
Implementing the following checklist will expedite and focus the approach:
- Confirm the total number of potential claims.
- Consider all possible policy exclusions.
- Obtain all CDC, OSHA, and public health and safety investigative reports.
- Confirm jurisdictional statutes for CO detectors.
- Identify other potential parties for contribution or indemnification.
- Obtain each plaintiff’s medical records, complete medical history, educational records, past and present employment histories, and social media involvement.
- Consult legal counsel with experience in CO exposure cases in order to properly assess the case, plaintiff’s counsel, and plaintiff’s experts and to engage the best available defense expert witnesses.