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Phenanthrene Syntheses

Haworth Synthesis

The Haworth Synthesis was published in 1932. This reaction involves a Friedel-Crafts acylation between naphthalene and succinic anhydride as well as two Clemmensen reductions and followed by a dehydrogenation with using the metal selenium.

Alternative Synthesis

In addition to the Haworth synthesis, there is an alternative synthesis which involves the dehydration cycloaromatization of an aldehyde. This synthesis involves [1,​1'-​Biphenyl]​-​2-​acetaldehyde reacting with triflic acid and hexafluoroisopropanol as the solvent.

Reactions

Phenanthrene's 9 and 10 bond is reactive and halogenation (i.e the addition of a halogen) easily happens. Shown below is the bromination of phenanthrene upon the 9 and 10 bond.

Chemical Properties

Physical Characteristics

Do to the molecule being non-polar and consisting of only carbon and hydrogen, phenanthrene is soluble in organic solvents such as carbon tetrachloride and toluene.

Chemical Characteristics

Phenanthrene's enthalpy of combustion and formation are calculated to be -(7048.7 ± 0.9) kJ/mol and (201.7 ± 2.9) kJ/mol, respectively.

Toxicity

Aquatic Toxicity

Phenanthrene has been discovered in contaminated seafood and surface water. As it is is highly lipid-soluble, it is easily metabolized and exerted by fish and invertebrates. Phenanthrene's lipid solubility contributes to it being able to bioaccumulate within the fatty tissues of organisms. Thus, the concentration of phenanthrene within in the organisms tissues will continue to increases as ingestion of the molecule continues. Additionally, with its ability to bioaccumulate, there is an increasing worry about it being accumulated to critical concentrations at high trophic levels. Phenanthrene has been known to cause acute toxicity to aquatic life whether this be inhibition of growth or mortality.

Crustaceans

Phenanthrene is toxic to deep-sea crustaceans. The effects of phenanthrene toxicity to deep sea crustaceans was studied by Turner et al. Turner et al. published a study that examined the mortality rate of different deep-sea crustacean species (Janciella spinacauda and Euphausiidae) when exposed to phenanthrene. The studied focused on effects of phenanthrene at different concentrations and varying time lengths. Turner et al. found that the rate of mortality is proportional to the concentration of phenanthrene. As the concentration of phenanthrene Increased, the exposed groups of Janciella spinacauda and Euphausiidaehad increasing mortalities. However, visible signs of acute toxicity caused by phenanthrene on Euphausiidae was apparent after only 3 hours of exposure. When Janciella spinacauda is exposed for 48 hours, the rate of mortality is increased. This correlates with the idea that increased exposure time led to increased acute toxicity. For Euphausiidae, they were highly sensitive to phenanthrene. That species had a 100% mortality rate at lower concentrations of phenanthrene than the other studied species. In addition, there is only a slight difference in the mortality rate when Euphausiidae is exposed to phenanthrene for 48 hr instead of 36 hr. Euphausiidae, being severely sensitive to phenanthrene, had the highest mortality rates of 24, 55, and 61% when exposed for 24, 36, and 48 hours, respectively. The LC50 for Euphausiidae and Janciella spinacauda are reported as 81 μg/L and 320 μg/L. As phenanthrene bioaccumulates in fatty tissues, Janciella spinacauda and Euphausiidae had specific critical target lipid body burden (CTLBB) calculated, and both organisms were reported to have phenanthrene in their fatty tissues. For the exposure length of 36 hr, Euphausiidae and Janciella spinacauda had CTLBB levels of 20.1 μmol/g lipid and 62.1μmol/g lipid, respectively. These levels were associated to be the target lipid levels for these organisms because these concentrations of phenanthrene within the deep-sea crustaceans were the cause of death to the crustaceans. Phenanthrene causes major harm to the stability of organisms. Even after the exposure event is done, phenanthrene has accumulated within the fatty tissues of the organisms, and this will lead to greater toxic effects for the organisms as time passes.

Microalgae

In regards to microalgae, phenanthrene has been reported to inhibit the growth of microalgae. Chen et al. published a study in a scientific journal, Scientific Reports, that studied the toxic effects of phenanthrene at varying pHs in regards to the microalgae Chlorella salina. The toxicity of phenanthrene created an environment where the microalgae's growth was unfavorable. The study used two different methods, cell counting and fluorimetric measuring, to determine the amount of Chlorella salina present after being exposed to phenanthrene. The fluorimetric method used the fluorescence properties of chlorophyll within Chlorella salina to measure the amount remaining after being exposed to phenanthrene. The authors reported that there is a correlation between the inhibition of algae growth, the concentration of phenanthrene, and acidity of the water. Within this article, there is a figure that demonstrates the relationship between phenanthrene concentrations and the inhibition rates via the two methods cell count and fluorescence measurements. While demonstrating the effects of phenanthrene concentrations on the algae, the figure also includes how the the inhibition rates vary at different pH levels. As reported within the article, there is a general trend between the increasing concentration of phenanthrene and the inhibition rate of the microalgae. As phenanthrene concentration increases, the inhibition rate increases. Using the cell counting method, after 96-hour exposure to phenanthrene with a concentration of 3.00 mg/L and the water's pH level of 9, there was a 59% inhibitory rate. When exposed to phenanthrene at more acidic pH levels, there was an increase in the inhibition of cell growth of Chlorella salina. After a 96-hour exposure of Chlorella salina to phenanthrene concentration of 3.00 mg/L with the water's pH level of 6, there was a 94% inhibitory rate amongst the microalgae. As the pH level decreased, the EC50 decreased from 1.893 to 0.237 mg L-1. The cell counting method determined that the decrease in pH increased the toxic effects that phenanthrene had on Chlorella salina. Moreover, the fluorimetric method established a heavier reliance on the concentration of phenanthrene to inhibiting the cell growth of Chlorella salina because the fluorimetric method shows an immense increase in inhibition rates as the concentration of phenanthrene increased for every pH levels examined. The two measuring methods produced slightly different results, but there was an agreeance that increasing the concentration of phenanthrene will lead to greater inhibition of growth of the Chlorella salina. Therefore, phenanthrene has drastic negative effects on microalgae and will inhibit their growth.

Zebrafish

Within the article by Incardona et al., they reported damage of embryos caused by the toxic effects of phenanthrene. Phenanthrene disrupted cardiac function and eventually caused heart failure of the embryos. The disrupted cardiac function included changes within heart rate and heart rhythm. In reduction of heart rate, phenanthrene had a dose-dependent relationship. In exposure to increased concentrations of phenanthrene, zebrafish had severe bradycardia that eventually amounted to complete atrioventricular blockage. Due to the disrupted cardiac function and heart failures, zebrafish embryos exhibited secondary effects: physical deformities such as smaller eyes and deformed jaws. In the article, Figure 7 compares the exposed group to the control. It was easy to see the deformities caused by the toxic effects from phenanthrene. The exposed group had small eyes, deformed jaws, and accumulated an edema. Overall, exposure of phenanthrene led to cardiac morphogenesis, heart failure, and edema accumulation.