Impact of Firefighting Aqueous Film-Forming Foams on Human Cell Proliferation and Cellular Mortality

Abstract

Objective

Evaluate the toxic effects of Aqueous Film-Forming Foams used by firefighters for Class B fire suppression in human-derived kidney cells (HEK-293).

Methods

Three widely used AFFFs were collected from fire departments and were added to HEK-293 cells in various concentrations. Seventy-two hours post-treatment, cellular proliferation and toxicity were examined using commercially available kits.

Results

All AFFFs evaluated induced cellular toxicity and significantly decreased cell proliferation, even when cells were treated with concentrations 10-fold lower than the working concentration used for fire suppression.

Conclusion

Despite the reduced usage of PFAS-containing AFFFs in the firefighter work environment, the evaluated AFFFs demonstrated significantly altered cellular proliferation, while also inducing toxicity, indicating the presence of toxic compounds. Both stronger implementation of PFAS-containing AFFFs restrictions and robust evaluation of fluorine-free and next-generation AFFFs are warranted.

In Brief

Firefighters are routinely exposed to per- and polyfluoroalkyl substances (PFAS) through the use of Aqueous Film-Forming Foams (AFFFs) for the suppression of Class B fire, which derive from flammable and combustible liquids, such as gasoline and alcohol. The addition of surfactants and PFAS in the AFFFs allows them to form an aqueous film that can extinguish the fire, while also coating the fuel. As such, AFFFs are often used for fire extinction in airports and military bases.

Exposure to PFAS in the general population may arise from ingestion of contaminated food or water, usage of consumer products containing PFAS, such as non-stick cookware or stain resistant carpets and textiles, and inhalation of PFAS-containing particulate matter. Detection of increased serum PFAS concentrations has been linked to an elevated risk for kidney cancer in humans, and firefighters are known to have increased serum concentrations of certain PFAS after attending training exercises. In the same study it was also observed that the average urinary excretions of 2-butoxyacetic acid (2-BAA) a surfactant often added in AFFFs exceeded the reference limit of the occupationally unexposed population, ranging from 0.5 to 1.4 mmol/mol creatinine.

Furthermore, an increased risk of mortality from kidney cancer has been observed in firefighters compared to the U.S. population. The detrimental health effects of PFAS are exacerbated by their increased half-lives in humans. A recently published study examined the half-lives of short- and long- chained PFAS in the serum of 26 airport employees and observed a wide range of half-lives which was dependent on the length and chemical structure of each substance that was examined. Indicatively, the shortest half-life was described for perfluorobutanesulfonic acid (PFBS), while the linear isomer of perfluorooctanesulfonic acid (PFOS) had the longest half-life (average of 44 days and 2.93 years, respectively), findings which are in agreement with other sources in the literature.

One aspect of this phenomenon could be attributed to renal reabsorption, as humans actively transport PFAS in the proximal tubules. A recently published scoping review of 74 epidemiologic, pharmacokinetic, and toxicological studies examined the relationship between PFAS exposure and kidney-related health outcomes. It was observed that exposure to PFAS was associated with lower kidney function, including chronic kidney disease (CKD), and histological abnormalities in the kidneys, as well as alterations in key mechanistic pathways, that can induce oxidative stress, and metabolic changes leading to kidney disease.

The alarming number of studies showcasing the harmful health effects pertaining to PFAS exposure has led to the banning of the production of AFFFs containing highly toxic, long chain PFAS, such as perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) since 2015. However, this regulation is gradually being implemented across states and little is known about the toxicity of the next generation AFFFs. Based on the above, in the present study we evaluate cellular proliferation and toxicity in kidney-derived cells (HEK-293) that were exposed to three widely used AFFFs.

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Organic solvents and Multiple Sclerosis susceptibility

Abstract

Photo of dichloromethane (DCM) as stored by Irish Air Corps in 2015. DCM was banned in the EU in 2012.
Objective

We hypothesize that different sources of lung irritation may contribute to elicit an immune reaction in the lungs and subsequently lead to multiple sclerosis (MS) in people with a genetic susceptibility to the disease. We aimed to investigate the influence of exposure to organic solvents on MS risk, and a potential interaction between organic solvents and MS risk human leukocyte antigen (HLA) genes.

Methods

Using a Swedish population-based case-control study (2,042 incident cases of MS and 2,947 controls), participants with different genotypes, smoking habits, and exposures to organic solvents were compared regarding occurrence of MS, by calculating odds ratios with 95% confidence intervals using logistic regression. A potential interaction between exposure to organic solvents and MS risk HLA genes was evaluated by calculating the attributable proportion due to interaction.

Results

Overall, exposure to organic solvents increased the risk of MS (odds ratio 1.5, 95% confidence interval 1.2–1.8, p = 0.0004). Among both ever and never smokers, an interaction between organic solvents, carriage of HLA-DRB1*15, and absence of HLA-A*02 was observed with regard to MS risk, similar to the previously reported gene-environment interaction involving the same MS risk HLA genes and smoke exposure.

Conclusion

The mechanism linking both smoking and exposure to organic solvents to MS risk may involve lung inflammation with a proinflammatory profile. Their interaction with MS risk HLA genes argues for an action of these environmental factors on adaptive immunity, perhaps through activation of autoaggressive cells resident in the lungs subsequently attacking the CNS.

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Anecdotal evidence has been emerging for some time of potential illness clusters at Casement Aerodrome to which Multiple Sclerosis has now been added. We are calling for these potential clusters to be investigated by competent authorities.

Suspected illness clusters currently include.