SIGNIFICANCE OF MONITORING PAHS IN THE
ENVIRONMENT & THEIR EFFECTS ON HUMAN HEALTH

 

3.0 SIGNIFICANCE OF MONITORING PAHS IN THE ENVIRONMENT & THEIR EFFECTS ON HUMAN HEALTH

PAHs are hydrophobic compounds and their persistence in the environment is mainly due to their low water solubility and electro-chemical stability. Evidence suggest that the lipophilicity, environmental persistence and genotoxicity of PAHs increase as the molecular size of the PAHs increases up to four or five fused benzene rings (Cerniglia , 1992). According to Hartwell ¹⁸⁵ more than 200 compounds are tested as possible carcinogens. Among these 25% have been found tumerogenic and about 30% of these were PAH (S.I. Lomb et al , 1980) have reported that BaP is a definite carcinogen with an LD50 of 24 micrograms. Many natural and anthropogenic source of PAHs in combination with global transport phenomenon result in the world-wide distribution of these compounds. About 500 PAHs have been detected in air, but most measurements have been made on BaP.

At present, no limit of PAHs either in air or in water environment has been prescribed in India. Also there is not any provision of granting consent based upon these compounds in the effluent and emissions from the stationary and mobile sources. Measurement of PAHs is helpful in assessing the existing level of PAHs in source emissions, ambient air, effluents, surface water, sludge/sediment. This will help in the development of data bank of PAHs levels in water and air, formulation and development of standards for ambient air quality, surface water, source emissions and effluents, granting consent based on PAHs to the relevant sources, identification and record of sources of PAHs and formulations of abatement and control strategies of PAHs in the environment.

3.1 Relative Potencies of Certain Mixtures:

Concentrations of BaP in natural petroleum crudes, retorted shale oils, coal-derived liquids and other sources are quite variable. It is estimated that 19 per 10,0000 exposed people may die from cancer of the respiratory tract as a result of spending a life time in ambient air containing an average level of BaP 1 ng per m³ mixed with all the other PAH from coke, oven and cigarette smoke emission. Relative potencies of certain mixtures are given below in Table -11 .

Table 11 : Relative Potencies of Certain Mixtures

For example, the BaP content of wood smoke has been estimated to range between 1 and 29 [mg BaP/g of mixture] (Ward 1999). Inserting all quantities into the above equation leads to a unit risk for wood smoke in the range of (0.07-1.9) x 10^-7 [µg/m³]^-1. If the BaP content of other mixtures are known the unit risk can be estimated in a similar way.

3.2 PAHs as Potential Carcinogens :

Evidence that mixtures of PAHs are carcinogenic to human comes primarily from occupational studies of workers following inhalation and dermal exposure. No data are available for human for the oral route of exposure. In the past, chimneysweepers and tar-workers were dermally exposed to substantial amounts of PAHs and PAHs caused skin cancer in many of these workers. Coke -oven workers, coal-gas workers and employees in aluminium production plants provide sufficient evidence of role of inhaled, PAHs in the induction of lung cancer.

As per USEPA report (1984) extensive epidemiological studies of coke oven workers , it was found that workers exposed to coke oven emissions were at an increased risk of cancer. A dose-response relationship was established in terms of both length of employment and intensity of exposure according to work area at the top or side of the coke oven. The relative risk of lung, trachea and bronchus cancer mortality in 1975 was 6.94 among Allegheny County, Pennsylvania coke oven workers who had been employed 5 or more years through 1953 and worked full time topside at the coke ovens. By comparison, side oven workers employed more than 5 years and followed through 1975 had a relative risk of 1.91, while non oven workers employed more than 5 years had a relative risk of 1.11. Sakable et al. (1975) observed a significant (P < 0.05) excess of lung cancer deaths (lung cancer mortality ratio of 2.37) among retired iron and steel coke oven workers in Japan when compared to expected which was derived from general population statistics. Mutagenicity tests on the complex mixture of solvent-extracted organics of coke oven emissions were positive in bacteria. A complex mixture from the coke oven collecting main was mutagenic in bacteria and mammalian cells in vitro. In addition, a number of components identified in coke oven emissions are recognised as mutagens and/or carcinogens.

A number of approaches are used to estimate the human lifetime respiratory cancer death due to a continuous exposure of 1 µg/m³ of the Benzene soluble organics (BSO) extracted from the particulate phase of CTPV from coke ovens emissions.

Using a Weilbull type model it is estimated that the risk due to a 1 µg/m³ unit exposure ranges from 1.30 x 10^-8 for the 95% lower-bound zero lag-time assumption to 1.05 x 10^-3 for the 95% upper-bound 15 year lag-time assumption. Using a multistage-type model, the maximum likelihood estimates for the risk due to unit exposure range from 1.76 x 10^-6 for the zero lag-time case of 6.29 x 10^-4 for the 15 year lag-time case.

Some PAHs are classified as potent carcinogens. The benzo (a) pyrene is referred to as " one of the most potent carcinogens known" in a recent publication by Sutherland et al (1995). PAHs are highly lipid-soluble and are absorbed by the lungs and gut of mammals. PAHs may penetrate into the bronchial epithelium cells where metabolism takes places.The carcinogenicity of individual PAC requires metabolic activations and conversion into their corresponding ultimate carcinogenic metabolites which are responsible for DNA alkylation and the initiation step in the complex mechanism, associated with chemically induced cancer.The PAH epoxide metabolites are products of P-450 catalysed reactions and one particular is enzyme P.450 01 A1 plays an important role in metabolite activation of several carcinogenic PAH (Harris et al. 1988; Dipple & Bigger, 1991). PAHs

are metabolised via the mixed -function oxidase system with oxidation as the first step. The resultant epoxides or phenols may go through detoxification reactions. Some epoxides can be further oxidized to diol-epoxide. These compounds are thought to be ultimate carcinogens. BaP is metabolised to approximately 20 primary and secondary oxidized metabolites. Several of these can induce mutations transform cells and /or bind to cellular macromolecules. A number of PAH have been shown to be mutagenic in bacterial systems and in vitro cell lines and in vivo by sister chromatid exchange. Sufficient evidence for activity in short-term test exist for six PAHs benz(a)anthracne, benzo)(a)pyrene, Cyclepenta(cd) pyrene dibenz(a,c) anthracene, dibenz(a,h) anthracene and 1-methylpenanthrene.

According to Hartwell more than 200 compounds are tested as possible carcinogens. Among these 25% have been found tumerogenic and about 30% of these were PAH. Lomb et al have reported that Bap is a definite carcinogen with an LD50 of 24 micrograms. International Agency on Cancer research (IARC, Lyon, France ) has classified PAH compound as follows:

Classification of Selected PAH's According to Carcinogencity (IARC, 1987)

Hoffman et al has listed the Potential Carcinogenicity and Bioactivity of the PAH as given in Table- 12.

Table-12: Potential Carcinogenicity and Bioactivity of PAH

Note : + to +++ Active, CC = Carcinogen with BaP , TI = Tumor initiator, C = Complete Carcinogen , 0 = Inactive.

The portion of the total carcinogenic effect of BaP in various particulate emissions is shown in Table-13

Table – 13 Portion of Carcinogenic Effect of BaP Related to Total Carcinogenicity

^aPreliminary results , as yet unfinished.

Source : A. Bjorseth, in Polynuclear Aromatic Hydrocarbons (P. W. Jones and P. Leber, Eds.), Ann Arbor Science Publishers, Ann Arbor, Michigan, pp. 371-381 ( 1979).

Thus, it is not enough to define the BaP content of a sample only. It is important to record a total profile of all carcinogens. These are, e.g., in automobile exhaust gas condensate, other PAH which in all represent 90% of the tumorigenic effect of the condensate.The serious health effects, caused from acute and chronic human exposure to PAH are of concern. These health effects include carcinogenesis, localized skin effects, pulmonary and respiratory problems, genetic reproduction and development effects, behavioural neurotoxic and other organ system effects. Several studies have been done on the PAHs in general and Benzo(a) Pyene in particular for their carcinogenic effect, solubilities in body fluids and plasma proteins. Benzo(e) Pyrene . The PAHs with 4-5 rings e.g. benezo(b) fluoroanthene and dibenzoanthracene have been recognized as directly carcinogenic. Other group of PAHs, for example chrysene, pyrene and fluoroanthene seem to have a potentating rather than direct effect.

Using the potencies of other non-heterocyclic polycyclic hydrocarbons relative to BaP (see Table AI.9 of EHC 202, WHO 1998i), unit risks can also be given as a rough estimate for these compounds by using of the formula .

UR_compound = (potency of compound)/(potency of BaP) x UR_BaP

Table -14 Estimate of Unit Risks for Several Polycyclic Aromatic Hydrocarbons

Source : WHO Guidelines for air pollutants with carcinogenic health endpoints

Annual mean concentration of BaP as measured in 1950s and 1960s in European cities ranged from 1 to over 100 ng/m³ the highest being found where coal was widely used for domestic heating. A value of 0.71% BaP in benzene-soluble coke-oven emissions would yield a lifetime risk of respiratory cancer of 8.7x10-5 per ng BaP per m³. According to USEPA, estimated risk of respiratory tract cancer ranges from 0.11x10^-5 to 1.4x10^-5 per ng BaP per m^3.