The concentration of carcinogenic poly aromatic hydrocarbons (c-PAHs) present in water and sediment of Klang Strait as well as in the edible tissue of blood cockle (Anadara granosa) was investigated. The human health risk of c-PAHs was assessed in accordance with the standards of the United States Environmental Protection Agency (US EPA). The cancer risks of c-PAHs to human are expected to occur through the consumption of blood cockles or via gastrointestinal exposure to polluted sediments and water in Kalng Strait. The non-carcinogenic risks that are associated with multiple pathways based on ingestion rate and contact rates with water were higher than the US EPA safe level at almost all stations, but the non-carcinogenic risks for eating blood cockle was below the level of US EPA concern. A high correlation between concentrations of c-PAHs in different matrices showed that the bioaccumulation of c-PAHs by blood cockles could be regarded as a potential health hazard for the consumers.
Concentration, source, and ecological risk of polycyclic aromatic hydrocarbons (PAHs) were investigated in 22 stations from surface sediments in the areas of anthropogenic pollution in the Klang Strait (Malaysia). The total PAH level in the Klang Strait sediment was 994.02±918.1 µg/kg dw. The highest concentration was observed in stations near the coastline and mouth of the Klang River. These locations were dominated by high molecular weight PAHs. The results showed both pyrogenic and petrogenic sources are main sources of PAHs. Further analyses indicated that PAHs primarily originated from pyrogenic sources (coal combustion and vehicular emissions), with significant contribution from petroleum inputs. Regarding ecological risk estimation, only station 13 was moderately polluted, the rest of the stations suffered rare or slight adverse biological effects with PAH exposure in surface sediment, suggesting that PAHs are not considered as contaminants of concern in the Klang Strait.
The distribution, sources, and human health risk assessment of polycyclic aromatic hydrocarbons (PAHs) in surface sediment and the edible tissue of short-neck clam (Paphia undulata) from mudflat ecosystem in the west coast of Malaysia were investigated. The concentrations of ∑16 PAHs varied from 347.05 to 6207.5 and 179.32 to 1657.5 ng g-1 in sediment and short-neck clam samples, respectively. The calculations of mean PEL quotients (mean-PELQs) showed that the ecological risk of PAHs in the sediment samples was low to moderate-high level, whereas the total health risk through ingestion and dermal contact was considerably high. The PAHs biota sediment accumulation factors data for short-neck clam were obtained in this study, indicating a preferential accumulation of lower molecular weight PAHs. The source apportionment of PAHs in sediment using positive matrix factorization model indicated that the highest contribution to the PAHs was from diesel emissions (30.38%) followed by oil and oil derivate and incomplete coal combustion (23.06%), vehicular emissions (16.43%), wood combustion (15.93%), and natural gas combustion (14.2%). A preliminary evaluation of human health risk using chronic daily intake, hazard index, benzo[a]pyrene-equivalent (BaPeq) concentration, and the incremental lifetime cancer risk indicated that PAHs in short-neck clam would induce potential carcinogenic effects in the consumers.
Polycyclic aromatic hydrocarbons (PAHs) are persistent pollutants and chemically a class of structurally similar chemical compounds characterized by the presence of fused aromatic rings. This research was undertaken to find out immunotoxic effects produced by pyrene, phenanthrene and fluoranthene. These chemicals were injected into developing chicks at three dose levels (0.2, 2 and 20 mg per kg) through allantioc route to rule out possible mechanisms involved in immunotoxicity. DNA adduct produced by PAHs in immune organs were analyzed by DNA adduct enzyme-linked immunosorbent assay (ELISA) kit and DNA damage was assessed by comet assay. A significant increase in the DNA adduct levels was found in thymus and bursa in 2 mg and 20 mg dose levels of pyrene, fluoranthene and phenanthrene treated groups, whereas those in spleen simulated the value of controls. Comet assay indicated that PAHs especially pyrene, fluoranthene and phenanthrene were capable of inducing increased level of comet parameters in thymus at all the dose levels. Bursa of Fabricius and spleen also showed a gradual rise in comet parameters corresponding to all dose levels, but the increase was more marked as in thymus. Thus, it can be concluded that DNA adducts produced by PAHs lead to single-strand breaks and reduced DNA repair, which ultimately begin a carcinogenic process. Hence, this experiment can be considered as a strong evidence of genotoxic potential of PAHs like pyrene, phenanthrene and fluoranthene in developing chicks.