Study on spatiotemporal distribution and health risk assessment of BTEX in urban ambient air of Kolkata and Howrah, West Bengal, India: Evaluation of carcinogenic, non-carcinogenic and additional leukaemia cases

Excessive exposure to benzene has been known for more than a century to damage the bone marrow resulting in decreases in the numbers of circulating blood cells, and ultimately, aplastic anemia. Of more recent vintage has been the appreciation that an alternative outcome of benzene exposure has been the development of one or more types of leukemia. While many investigators agree that the array of toxic metabolites, generated in the liver or in the bone marrow, can lead to traumatic bone marrow injury, the more subtle mechanisms leading to leukemia have yet to be critically dissected. This problem appears to have more general interest because of the recognition that so-called “second cancer” that results from prior treatment with alkylating agents to yield tumor remissions, often results in a type of leukemia reminiscent of benzene-induced leukemia. Furthermore, there is a growing literature attempting to characterize the fine structure of the marrow and the identification of so called “niches” that house a variety of stem cells and other types of cells. Some of these “niches” may harbor cells capable of initiating leukemias. The control of stem cell differentiation and proliferation via both inter- and intra-cellular signaling will ultimately determine the fate of these transformed stem cells. The ability of these cells to avoid checkpoints that would prevent them from contributing to the leukemogenic response is an additional area for study. Much of the study of benzene-induced bone marrow damage has concentrated on determining which of the benzene metabolites lead to leukemogenesis. The emphasis now should be directed to understanding how benzene metabolites alter bone marrow cell biology.

Over the past three decades, China has experienced rapid urbanization. The risks to its urban population posed by inhalation exposure to hazardous air pollutants (HAPs) have not been well characterized. Here, we summarize recent measurements of 16 highly prevalent HAPs in urban China and compile their distribution inputs. Based on activity patterns of urban Chinese working adults, we derive personal exposures. Using a probabilistic risk assessment method, we determine cancer and non-cancer risks for working females and males. We also assess the uncertainty associated with risk estimates using Monte Carlo simulation, accounting for variations in HAP concentrations, cancer potency factors (CPFs) and inhalation rates. Average total lifetime cancer risks attributable to HAPs are 2.27×10(-4) (2.27 additional cases per 10,000 people exposed) and 2.93×10(-4) for Chinese urban working females and males, respectively. Formaldehyde, 1,4-dichlorobenzene, benzene and 1,3-butadiene are the major risk contributors yielding the highest median cancer risk estimates, >1×10(-5). About 70% of the risk is due to exposures occurring in homes. Outdoor sources contribute most to the risk of benzene, ethylbenzene and carbon tetrachloride, while indoor sources dominate for all other compounds. Chronic exposure limits are not exceeded for non-carcinogenic effects, except for formaldehyde. Risks are overestimated if variation is not accounted for. Sensitivity analyses demonstrate that the major contributors to total variance are range of inhalation rates, CPFs of formaldehyde, 1,4-dichlorobenzene, benzene and 1,3-butadiene, and indoor home concentrations of formaldehyde and benzene. Despite uncertainty, risks exceeding the acceptable benchmark of 1×10(-6) suggest actions to reduce exposures. Future efforts should be directed toward large-scale measurements of air pollutant concentrations, refinement of CPFs and investigation of population exposure parameters. The present study is a first effort to estimate carcinogenic and non-carcinogenic risks of inhalation exposure to HAPs for the large working populations of Chinese cites.