Polycyclic Aromatic Hydrocarbons: Environmental Sources, Associations with Altered Lung Function, and Potential Mechanisms
Polycyclic aromatic hydrocarbons (PAHs) represent a large class of organic compounds characterized by two or more fused benzene rings arranged in diverse configurations. With hundreds of identified variants, PAHs are pervasive environmental pollutants generated through incomplete combustion of carbon-containing materials. While natural sources like volcanic eruptions and wildfires contribute to PAH emissions, anthropogenic activities—including industrial processes, vehicular exhaust, cigarette smoke, residential heating fuels, and high-temperature food preparation methods such as grilling and frying—account for the majority of atmospheric PAH contamination. These compounds enter the human body via inhalation, ingestion, and dermal contact, with urinary monohydroxylated PAH metabolites (OH-PAHs) serving as reliable biomarkers for assessing individual exposure levels.
Environmental Sources and Exposure Pathways
PAH exposure varies significantly across populations, influenced by environmental and lifestyle factors. Traffic emissions remain a dominant outdoor source, contributing approximately one-eighth of global PAH emissions. Indoor environments, however, present heightened risks due to cigarette smoke, which contains over 500 distinct PAHs. Notably, cigarette smoke generates PAH levels 1.5 to 4 times higher than other indoor combustion sources. For non-smokers and non-occupational groups, dietary intake emerges as a primary exposure route. Crops like rye, wheat, and lentils absorb PAHs from air, water, or soil, while cooking methods such as smoking, grilling, and frying introduce substantial PAHs into food. Cooking fumes, in particular, release PAHs that are readily inhaled.
Population-specific studies highlight the variability in PAH exposure. For example, children exposed to household smoking exhibited elevated urinary levels of 2-hydroxyfluorene (2-OHFlu), 9-hydroxyfluorene (9-OHFlu), and 1-hydroxypyrene (1-OHP). Similarly, gas-based cooking appliances increased urinary 2-OHFlu, 9-OHFlu, and hydroxyphenanthrene metabolites (1-OHPh, 3-OHPh), while coal or wood heating raised 1-OHP levels. In Korea, non-smoking women residing near major roads showed higher urinary 2-OHFlu and 1-OHPh, underscoring traffic-related exposure. Iranian adults exposed to insecticides, tar products, or candle burning displayed elevated 1-hydroxynaphthalene (1-OHNa) and 2-hydroxynaphthalene (2-OHNa).
A large-scale study of 4,092 urban Chinese residents further delineated exposure sources. Cigarette smoking significantly correlated with increased urinary 1-OHNa, 2-OHNa, and 2-OHFlu. Dietary PAH intake raised 1-OHNa, 2-OHNa, and 9-OHFlu levels, while prolonged traffic exposure (>30 minutes daily) elevated 9-OHFlu and 1-OHPh. Home-cooking activities were linked to higher 1-OHP, though improved kitchen ventilation reduced low-molecular-weight OH-PAHs. Crucially, smoking exhibited synergistic effects when combined with other exposure sources, amplifying urinary metabolite concentrations.
PAH Exposure and Lung Function Decline
Both occupational and general populations demonstrate associations between PAH exposure and impaired lung function. In a 4-year study of 1,243 coke oven workers, baseline urinary OH-PAH levels inversely correlated with declines in forced expiratory volume in one second (FEV1), forced vital capacity (FVC), and mid-expiratory flow rates (FEF25–75). For instance, each 1-unit increase in log-transformed total OH-PAHs corresponded to a 37.13 mL reduction in FEV1.
General population studies corroborate these findings. Among 2,747 Chinese adults, elevated urinary OH-PAHs—including 2-OHNa, 2-OHFlu, and hydroxyphenanthrene derivatives—were associated with significant FEV1 and FVC declines. For example, 2-OHNa exposure reduced FEV1 by 23.79 mL and FVC by 24.39 mL per log-unit increase. Particulate matter (PM2.5)-bound PAHs, such as naphthalene, fluoranthene, and pyrene, exacerbated lung function loss over time. Long-term exposure to high-molecular-weight PAHs like benzo[a]anthracene and dibenzo[a,h]anthracene led to FVC reductions exceeding 200 mL over three years.
Mechanisms Underlying PAH-Induced Lung Damage
PAHs exert detrimental effects through oxidative stress, inflammation, and compromised lung epithelial integrity. Metabolic activation of PAHs by cytochrome P450 enzymes generates reactive oxygen species (ROS), which damage DNA, lipids, and proteins. Urinary biomarkers like 8-hydroxy-2′-deoxyguanosine (8-OHdG) and 8-isoprostane (8-iso-PGF2α) reflect oxidative DNA and lipid damage, respectively. In the Wuhan-Zhuhai cohort, oxidative stress mediated 22.13% of the association between high-molecular-weight OH-PAHs and FVC decline.
Persistent inflammation further exacerbates lung dysfunction. PAHs stimulate pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6, which promote airway hyperresponsiveness and remodeling. Epidemiological studies link PAH exposure to elevated C-reactive protein and immune cell activation, both correlated with lung function deterioration.
Club cell secretory protein-16 (CC16), a biomarker of lung epithelial integrity, plays a protective role. Reduced plasma CC16 levels correlate with accelerated FVC decline in individuals with high PAH exposure. Over three years, subjects with low CC16 experienced significant lung function loss when exposed to elevated PAHs, highlighting CC16’s role in mitigating oxidative and inflammatory damage.
Implications for Public Health
The ubiquity of PAHs in urban environments necessitates targeted interventions. Reducing traffic emissions, promoting smoke-free households, and improving kitchen ventilation can lower exposure. Public awareness campaigns on dietary choices—such as avoiding charred foods—may further mitigate risks. Occupational safeguards, including regular health monitoring and enhanced workplace air quality, are critical for high-risk groups.
Conclusion
PAHs, arising from diverse combustion sources, pose significant threats to respiratory health through oxidative stress, inflammation, and epithelial damage. Urinary OH-PAHs provide a robust tool for exposure assessment, while biomarkers like CC16 offer insights into individual susceptibility. Addressing PAH emissions through policy and lifestyle changes remains essential to safeguarding lung function and reducing the burden of respiratory diseases.
doi.org/10.1097/CM9.0000000000000880
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