In order to evaluate the exposure of the northern India rural population to polyaromatic hydrocarbon (PAH) inhalation, indoor pollution was assessed by collecting and analyzing the respirable particulate matter PM2.5 and PM10 in several homes of the village Bhithauli near Lucknow, UP. The home selection was determined by a survey. Given the nature of biomass used for cooking, homes were divided into two groups, one using all kinds of biomass and the second type using plant materials only. Indoor mean concentrations of PM2.5 and associated PAHs during cooking ranged from 1.19±0.29 to 2.38±0.35 and 6.21±1.54 to 12.43±1.15 μg/m3, respectively. Similarly, PM10 and total PAHs were in the range of 3.95±1.21 to 8.81±0.78 and 7.75±1.42 to 15.77±1.05 μg/m3, respectively. The pollutant levels during cooking were significantly higher compared to the noncooking period. The study confirmed that indoor pollution depends on the kind of biomass fuel used for cooking.

Asbestos is a known carcinogen and co-carcinogen. It is a persisting risk in our daily life due to its use in building material as asbestos-cement powder. The present study done on V79-cells (Chinese hamster lung cells) demonstrates the cytotoxic and genotoxic potential of asbestos-cement powder (ACP) in comparison with chrysotile asbestos. A co-exposure of chrysotile and ACP was tested using the cell viability test and the micronucleus assay. The kinetochore analysis had been used to analyse the pathway causing such genotoxic effects. Thiobarbituric acid-reactive substances were determined as evidence for the production of reactive oxygen species. Both, asbestos cement as well as chrysotile formed micronuclei and induced loss of cell viability in a concentration-and time-dependent way. Results of TBARS analysis and iron chelator experiments showed induction of free radicals in ACP-and chrysotile exposed cultures. CaSO 4 appeared to be a negligible entity in enhancing the toxic potential of ACP. The co-exposure of both, ACP and chrysotile, showed an additive effect in enhancing the toxicity. The overall study suggests that asbestos-cement is cytotoxic as well as genotoxic in vitro. In comparison to chrysotile the magnitude of the toxicity was less, but co-exposure increased the toxicity of both.

Asbestos was monitored in water, sediment, and aquatic plant samples around an asbestos cement factory. Based on asbestos concentration found in aquatic plants during monitoring, and the propensity of asbestos to cause oxidative stress in animal models, laboratory experiments were conducted to assess toxicity of chrysotile asbestos on an aquatic macrophyte, duckweed (Lemna gibba). L. gibba plants were exposed to two concentrations of chrysotile asbestos (0.5 microg and 5.0 microg chrysotile in 5.0 microl double distilled water) twice per week during a period of 28 days and cultured in medium containing 0.1 g chrysotile/L. Control plants were cultured in medium without chrysotile asbestos. Effect of chrysotile exposure on certain growth and physiological and biochemical parameters was evaluated. An inhibition effect of chrysotile exposure was found on the number of fronds, root length, and biomass. Similar alterations in contents of chlorophyll, carotenoid, total free sugar, starch, and protein were also found. Contrary to effect on these parameters, a dose- and time-dependent increase in efflux of electrolytes, lipid peroxidation, cellular hydrogen peroxide, catalase, and superoxide dismutase activity was found. The results indicate oxidative stress and phytotoxicity of chrysotile asbestos on duckweed.

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