Interior Use of Positive Pressure – Part 1
Related Debate at The Kitchen Table: Food for Thought on PPV
AP Photo/Mike Meadows
Firefighters try to ventilate windows as smoke pours from a five-story office building in the Hollywood section of Los Angeles on Dec. 18, 1999.
While current research suggests that positive pressure ventilation, especially in high-rise structures, can be more effective when fans are used inside, considerable resistance continues to exist in the firefighting community. The most common argument against the use of PPV inside structures is that it creates a carbon monoxide hazard. But I argue that in order to maximize our ability to save lives at high-rise fires, we should reconsider our resistance to taking the fans inside.
Smoke is killing many more people than flames are. If we want to save lives, we have to get the smoke out. In high-rise firefighting scenarios, this becomes even more crucial as available ventilation options are limited and the enclosed stairs, the primary means of egress, act as chimneys for smoke travel.
I would suggest that we use a rational science-based approach to managing toxic inhalation exposure during and immediately after firefighting operations for both firefighters and civilians using a fully informed risk benefit analysis. Given what we currently know about fire and smoke and coupled with available technology, we can use CO levels inside a structure as the toxic exposure benchmark but hopefully at levels more appropriate to what the literature suggests and not at the pre-set alarm level of a given meter.
The fireground poses many dangers, not least of which is exposure to any number of toxic chemicals that are the natural byproducts of the combustions of both natural and synthetic materials. The number of possible exposure chemicals is too numerous to develop monitoring metrics for. However, CO is present at all fires and more importantly is easily measured using standard off-the-shelf metering products.
Assuming the use of gas-powered fans, the rationale then follows that by effectively using PPV or some other form of ventilation we can quickly lower the concentration of the unknown smoke hazards, leaving us to manage the CO produced by the fan. CO is a hazard we know, can treat if necessary and can easily quantify.
The increased prevalence of electric PPV fans is lessening the impact of fire department-induced CO on fire ground operations. However, there are still gas PPV fans everywhere and they can be expected to remain in service for the foreseeable future. By developing a sound risk/benefit paradigm, firefighters can reduce their exposure and the exposure of civilians exposed to fire. In turn, this will reduce the risk of injury that the heat stress and cardiac stress of a fully dressed firefighter causes.
Sufficient research exists to have a reasonably firm idea of both the acute and chronic effects of CO. What drives the need for change is research conducted by the National Institute of Science and Technology, which supports the benefits of PPV. This is even with gas blowers, noting that the highest experimentally attainable interior stairwell CO level (with the stair door open) is 50-80 PPM and at least one order of magnitude less than the amounts created by the fire.
It would take a considerable amount of time to review the full breadth of data available on CO exposure and poisoning. However, even in this limited review, some common themes become available:
• An inability to isolate CO as the primary cause of illness
• Uncertainty about what levels over what time frame denote “chronic exposure”
• Those who are already impaired, either from cardiac or respiratory issues are at increased risk
• Those who are either very young or very old are also at increased risk
• CO poisoning can be reversed most times with few lingering effects
The periods during initial attack, immediate post knock-down, and after full extinguishment are times during the fire work cycle where there is no real exposure to CO because the firefighters are wearing their SCBA.
CO is an odorless, colorless and tasteless gas that is the by-product of incomplete combustion. It is present in ambient air, with noticeable increasing in areas where there is a large volume of vehicular traffic (Fierro, 2001), prescribed burns (Slaughter, 2004), or obviously in structure fires. Fierro states that, “The majority of the population is exposed to low ambient concentrations of CO resulting in an average blood concentration of carboxyhemoglobin of less than 2%.” Furthermore she notes that, "…in many American cities, high short-term peak CO concentrations (mean 50ppm) occur in heavy traffic areas.” The mitigating factor in this discussion is the exposure time. Fierro’s discussion is based primarily of persons who are exposed to that dose over an extended period of time, i.e., a workday.
We are exposed to 50ppm on a hot summer day working a crash on the Interstate but balk at 35ppm inside a house that was on fire.
The difficulty comes in translating these doses into the type of exposure typical for the firefighter. During firefighting operations, the peak CO output should occur during the incipient and smoldering phases of the fire. Most firegrounds are resolved in a matter of minutes, hours at most, with at least some portion of that time not being an exposure time for fire crews. The periods during initial attack, immediate post knock-down, and after full extinguishment are times during the fire work cycle where there is no real exposure to CO because the firefighters are wearing their SCBA.
Exposure to CO can be hazardous to health because CO is absorbed through the respiration. It moves quickly across the alveolar capillary membranes, eventually entering the bloodstream where it competes with oxygen for space on the hemoglobin molecule. Complicating matters is the fact that the affinity of hemoglobin for CO is nearly 300 times greater than it affinity for oxygen (Fierro, 2001). Studies suggest that, "…alteration in the cardiac autonomic function reflected in changes in HRV might play an important role in the pathophysiology of increased cardiovascular mortality in association with ambient air pollution” (Tarkiainen, 2003).
In cases where otherwise healthy adults have been exposed to high levels of CO, the outcomes have been promising. Ayers discusses many cases where people exposed to high CO levels over periods of up to 18 months have recovered their neurological losses rather quickly and without lasting impact (Ayers, 1998).
This discussion of effects is not to make the argument that CO is harmless to firefighters. However, the variety of the scope and depth of the literary investigations calls into question the standards by which fire departments determine the permissible levels that they do for fireground exposures. For example, the neuro deficit caused and discussed in the Ayers study involved eight-hour exposures to 100PPM of CO.
This exposure is outside the scope of reasonable for the average firefighter. And while everyone can agree that the wildland firefighter is probably exposed more often to higher concentrations of smoke, the decreased lung function found in the Slaughter study could not be conclusively linked to CO. Slaughter concluded, "…that the prescribed burn smoke exposures were associated with significant pre- to post-shift decreases in lung function…Our analysis was not able to identify any single component of the smoke that was significantly associated with the lung decrements.”. The point is we know that CO causes harm, but we cannot say that the harm we suffer after a fire is related to CO.
This inability to pinpoint causation flies in the face of the non-scholarly articles found in the typical fire department publications, which tend not to be either juried or based on sound, reproducible scientific methodology. These reports strike fear using dramatic titles such as “Carbon Monoxide: An Insidious Menace” (Shouldis, 2004). Shouldis does not present any scientific data to support his case review with the exception of a chart outlining the adverse health effects of CO.
Unfortunately the scientists are not as confident. Carlin points out that, "…estimation of the maximal level of carbon monoxide exposure cannot be accurately determined…” (Carlin, 1999). In other words, we cannot go backwards from blood CO levels to determine the amount of exposure present. The ability to isolate CO is severely limited. And in cases where the concentration of exposure is known, there is no reliable way to predict any given person’s reaction to that concentration.