Mutagenicity and carcinogenicity of combustion emissions are impacted more by combustor technology than by fuel composition: A brief review

Abstract

Studies during the past 50 years have characterized the carcinogenicity and mutagenicity of extractable organic material (EOM) of particulate matter (PM) in ambient air and from combustion emissions. We have summarized conclusions from these studies and present data supporting those conclusions for 50 combustion emissions, including carcinogenic potencies on mouse skin (papillomas/mouse/mg EOM), mutagenic potencies (revertants/μg EOM) in the Salmonella (Ames) mutagenicity assay, and mutagenicity emission factors (revertants/kg fuel or revertants/MJthermal) in Salmonella. Mutagenic potencies of EOM from PM in ambient air and combustion emissions span 1–2 orders of magnitude, respectively. In contrast, the revertants/m3 span >5 orders of magnitude due to variable PM concentrations in ambient air. Carcinogenic potencies of EOM from combustion emissions on mouse skin and EOM‐associated human lung cancer risk from those emissions both span ~3 orders of magnitude and are highly associated. The ubiquitous presence of polycyclic aromatic hydrocarbons (PAHs), nitroarenes, and aromatic amines results in mutagenic and carcinogenic potencies of PM that span only 1–3 orders of magnitude; most PM induces primarily G to T mutations. Mutagenicity emission factors of combustion emissions span 3–5 orders of magnitude and correlate with PAH emission factors (r > 0.9). Mutagenicity emission factors were largely a function of how material was burned (highly efficient modern combustors versus open burning) rather than what materials were burned. Combustion systems that minimize kinetic and mass‐transfer limitations and promote complete oxidation also minimize the mutagenicity of their emissions. This fundamental engineering principle can inform environmental and public health assessments of combustion emissions.

Mutagenicity of the organic fraction of World Trade Center dust

“…(Table 5, Figure 3), and it was 10 times lower than the lowest among the particles from 50 combustion emissions reviewed recently (DeMarini & Linak, 2022). As noted above, the SRM 1649b particles ranged from 0.2 to 100 μm, with a median size of 20 μm, and the WTC dust particles were <53 μm, resulting in an overlap in the size range between the two types of particles.…”

“…However, WTC dust EOM was 10 times more mutagenic in TA100 +S9 than in TA98 +S9 ( p < .0001), indicating that it was more potent as a base-substitution mutagen than as a frameshift mutagen ( Table 3 ). The requirement for S9 for the WTC EOM to be mutagenic in these strains and the greater potency in TA100 relative to TA98 suggest that PAHs likely accounted for much of this activity ( DeMarini & Linak, 2022 ). The mutagenic potency of the EOM of SRM 1649b was 25 times greater than that of WTC dust in TA98 +S9, and it was twice as mutagenic as that of the WTC dust EOM in TA100 +S9 ( p < .0001) ( Table 3 ).…”

“…Cupitt et al (1994) show the high correlation of these data with the carcinogenic potency of the EOMs on mouse skin, generating a standard curve from which an estimate of lung cancer risk can be made using the carcinogenic potency of EOMs on mouse skin. Such estimates have been made for air samples (Cupitt et al, 1994) and smoky coal emissions (DeMarini & Linak, 2022).…”

“…Among a wide array of combustion emissions, there is a Spearman r correlation of $1 between the mutagenicity emission factor (revertant/megajoule thermal ) and the PAH emission factor (μg PAH/ megajoule thermal ) (DeMarini & Linak, 2022). PAHs play a mechanistic role in the mutagenicity and carcinogenicity of PM in both rodents and humans, and the mutagenicity of the EOM from complex mixtures is a mechanistic component of the rodent and human carcinogenicity resulting from exposure to those mixtures (DeMarini & Linak, 2022;IARC, 2010IARC, , 2014IARC, , 2016.…”

After a Century of Research into Environmental Mutagens and Carcinogens, Where Do We Stand?

“…increasing expression and subsequent up-regulation of oncoproteins (see Ross and Nesnow [14]). Considering the prevalence of PAHs in emissions such as tobacco smoke plus fumes and their particulate matter, this issue has been receiving specific attention due to its implications in human lung cancer (reviewed by Moorthy et al [15], DeMarini and Linak [16]). The paradigmatic case study of PAH mutagenicity and carcinogenicity illustrates that cell and molecular biology laid important foundations for establishing causation and both human and ecological risk assessment.…”