|Abstract or Summary
- In recent decades, there has been increased attention on human exposure to, and subsequently toxicity of, Polycyclic Aromatic Hydrocarbons (PAHs). PAHs are widespread organic pollutants and some have been shown to be toxic, carcinogenic and mutagenic. This research was focused on understanding the link between global PAH emissions and lung cancer risk, as well as the metabolism of PAHs by humans. We investigated human exposure to PAHs via inhalation and ingestion, their metabolism to hydroxy-PAHs (OH-PAHs) and compared the results to the OH-PAH concentrations in the general US population.
The objective of the first part of this research was to investigate the relationship between lung cancer mortality rates, carcinogenic PAH emissions, and smoking on a global scale. We also investigated this relationship in different socioeconomic country groups. The data from the World Health Organization provided two lung cancer mortality rates, including estimated lung cancer deaths per 100,000 people (ED100000) and age standardized lung cancer death rate per 100,000 people (ASDR100000) for 136 countries. Both mortality rates were regressed on PAH emissions in benzo[a]pyrene equivalence (BaPeq), smoking prevalence, cigarette price, gross domestic product per capita, percentage of people with diabetes, and average body mass index. Both simple linear regression and multiple linear regressions with stepwise procedure were used. The results showed a statistically significant positive linear relationship between log[subscript e](ED100000) and log[subscript e](BaPeq) emissions for high socioeconomic country group (p-value<0.01). Additionally, both log[subscript e](ED100000) and log[subscript e](ASDR100000) were significantly positively correlated with log[subscript e](BaPeq) emissions for the combination of upper middle and high (p-value<0.05) socioeconomic country groups.
The objective of the second part of this research was to investigate human inhalation exposure to PAHs. We developed a method for the measurement of 19 parent PAHs and 34 hydroxylated PAHs (OH-PAHs) in urine and particulate matter less than 2.5 um in diameter (PM₂.₅) using GC-MS. We validated this method using NIST SRM 3672 (Organic Contaminants in Smoker's Urine) and SRM 3673 (Organic Contaminants in Nonsmoker’s Urine). The method was used to measure PAHs and OH-PAHs in urine and personal PM₂.₅ samples collected during fish smoking activities at the Confederated Tribes of Umatilla Indian Reservation (CTUIR). Two different fish smoking facilities (tipi and smoke shed) were used and two different wood types (alder and apple) were burned. Urine samples were hydrolyzed, concentrated using solid phase extraction, and fractionated using silica phase to separate PAHs and OH-PAHs. The 34 OH-PAHs were derivatized using N-(t-butyldimethylsilyl)-N-methyltrifluoroacetamide (MTBSTFA), and both OH-PAHs and PAHs were measured by GC-MS. The personal PM₂.₅ samples were extracted using pressurized liquid extraction, derivatized with MTBSTFA and analyzed by GC-MS for PAHs and OH-PAHs. Isotopically labeled surrogates of PAHs and OH-PAHs were added to accurately quantify analytes. The results showed an increase in OH-PAH concentrations in urine after 6 hours of fish smoking and an increase in PAH concentrations in air within each smoking facility. In general, the PAH exposure in the smoke shed was higher than in the tipi and the PAH exposure from burning apple wood was higher than burning alder.
The objective of the third part of this research was to investigate human oral exposure to PAHs. We estimated excretion rates and half-lives of 4 PAHs and 10 OH-PAHs after the consumption of Native American traditionally smoked fish. Nine members of the CTUIR consumed smoked fish for breakfast and urine samples were collected during the following 24 hours. The results showed significant increase in OH-PAH concentrations 3 to 6 hr post-consumption. The lowest half-life was for retene (1.4 hr) and the highest was for 3-hydroxyfluorene (7.0 hr).