Cancer information mesothelioma

INVESTIGATORS HAVE copiously used risk assessment to bridge the intricate relationship between science and policy in the prioritization and control of hazardous materials, especially chronic health hazards and carcinogens.[1] Researchers have implemented four steps before they assess risk: (1) hazard identification, (2) dose-response assessment, (3) exposure assessment, and (4) risk characterization.[2] However, investigators have often questioned the validity of risk estimates in previous studies because there was an incomplete and/or inaccurate assessment of exposure and population at risk, and there was also an uncertain exposure-effect model.[3] Therefore, these difficulties must be resolved if any form of risk assessment can influence poi icy effectively.

Asbestos has been used widely as a raw material in more than 3 000 commercial products.[4] Given that asbestosis, pleural plaques, malignant mesothelioma, and lung cancer are associated with asbestos exposure,[5-7] investigators, during the past four decades, have conducted numerous studies that focused on occupational and nonoccupational exposure to asbestos.[8] Although asbestos concentrations in the general ambient air are relatively low,[9] the potentially greater exposure level to residents who live near asbestos factories is of great importance.

Approximately 30 000 tons of asbestos were consumed annually by the following types of factories in Taiwan:[10] 21 cement, 13 friction (brake production), 3 textile, 2 ground tile, 1 insulation, and 1 refractory. However, the wet-manufacturing process was used by only some of the asbestos cement and refractory factories. The average air concentrations of asbestos in these industries ranged between 2.1 fiber/ml and 6.3 fiber/ml[11]--levels potentially harmful to individuals who live in nearby neighborhoods.

Investigators have already demonstrated that workers in a forging factory[12] and kindergarten children[13] who attended a school located near a lead-recycling factory had significantly increased lead absorption and/or IQ impairment. These results have alarmed individuals who reside near asbestos factories. In addition to a very high population density (i.e., [is greater than] 580 persons/[km.sup.2]), Taiwan has poor zoning regulations between industrial and residential areas. The risk of contracting the two most common types of asbestos-related cancer--lung cancer and mesothelioma--from factory emissions is a critical issue. We therefore sought to determine the risk of lung cancer and mesothelioma among Taiwanese residents who lived near asbestos factories anytime after birth.

Materials and Method

Exposure assessment. We performed samplings in all 41 asbestos factories registered in Taiwan. Investigators visited each factory 1 d prior to sampling to draw schematics of each facility. The Taiwan Environmental Protection Agency, which requested the walk-throughs, asked investigators to also complete a questionnaire that contained information about emission control and waste management. We used satellite maps (1:5 000) of each asbestos factory to locate the sampling sites. The asbestos emission source of each factory was located, and concentric circles with diameters of 200 m, 400 m, and 600 m were plotted. We used a high-volume sampler (Aircheck sampler model 224-PCXR7 [Eighty Four, Pennsylvania]). We collected an 8-h sample at the upwind side--at least 1 000 m from the emission source of each asbestos factory--to ascertain the background level of asbestos exposure in the ambient atmosphere. The background sampling site was chosen on the basis of the following criteria: (a) no asbestos-related factories were within 1 000 m of the sampling site; (b) no observable asbestos material was at the site, including asbestos cement wall, roof, etc.; and (c) traffic intersections were at least 100 m from the site, thus avoiding potential asbestos fiber generated from brake friction. We used mixed cellulose ester filters (pore size = 0.8 [micro]m [Millipore type A]) to collect the asbestos fibers. The flow rate of sampling was set at 3 l/min, and calibration of flow rate was performed both before and after each sampling. We discarded samples if there was a 10% deviation between the flow rate noted before and after each sampling. At least two field blanks were prepared for each factory sampling. We used a cassette sealing band to prevent leakage from the cassette holder. Samples were stored upright in a sealed box, thus avoiding possible contamination during shipment.

We collected a total of 246 samples from 41 factories. Given the manpower and time constraints, we used stratified random sampling to examine only parts of the samples by transmission electronic microscopy (TEM). We followed analytic method number 7402 prescribed by the National Institute of Occupational Safety and Health (NIOSH).[14] The following factories were chosen randomly in each different strata: 5 of 21 cement factories, 3 of 13 friction factories, 2 of 3 textile factories, 2 ground-tile factories, 1 insulation factory, and 1 refractory factory. We measured 69 valid samples obtained from these factories by TEM, and the remainder of the samples were determined with phase-contrast microscopy (PCM).[15] We used TEM (Zeiss D-7082), equipped with an energy-dispersive x-ray analyzer (Kevex, model 3200-0400), and PCM (Olympus, Japan; 10 x 40) to determine airborne asbestos concentrations.

We sent one-tenth of TEM samples to the Environmental Science Laboratory (McGill University, Canada) for cross-check, thus assuring accuracy and precision of our electromicroscopic examinations.

Dose-response model for lung cancer. The dose-response curves for the relationship between asbestos and lung cancer were taken from previous epidemiological studies.[16-20] These curves were based on the following three assumptions: (1) there was no threshold effect, (2) the effect of cumulative exposure remained steady following 10 y of an induction period, and (3) risk was proportional to the product of duration and concentration of asbestos exposure.

Inasmuch as these curves resulted from occupational exposure settings--for which the annual exposure profile is 8 h/d, 5 d/wk, and 48 wk/y--adjustment for residential exposure was necessary. In Taiwan, individuals who lived near the factories were exposed to asbestos 16 h/d, 7 d/wk, for 50 wk/y. Therefore, the conversion factor between occupational and nonoccupational residential exposure was 50 x 16 x 7/(40 x 48) = 2.92. The formula for excess risk of lung cancer attributable to asbestos exposure can be expressed as follows:

D = O - E = E x (b/100) x X x w,

where D = excess deaths from lung cancer; O = observed deaths; E = expected deaths; X = cumulative exposure dose of asbestos (i.e., fibers/y [multiplied by] [cm.sup.3]); w = weighting factor or conversion factor; and b = slope (i.e., fibers/y [multiplied by] [cm.sup.3]), dependent on asbestos factory (asbestos cement: 0.5, asbestos textile = 3). Given the contradictory findings[21,22] and the absence of a model, we did not analyze the elevated risk of lung cancer for friction factories (Fig. 1).

[Figure 1 ILLUSTRATION OMITTED]

Dose-response model for mesothelioma. In human epidemiological studies, investigators have shown that the incidence of mesothelioma might be associated with asbestos fiber types (e.g., crocidolite and amosite cause higher incidence rates than chrysotile). These findings, however, remain inconclusive.[23-26] Moreover, Peto et al.[27] calculated that the incidence rate of mesothelioma in the general population is approximately 1 per million. The cumulative incidence rate of mesothelioma in Taiwan (up to age 74 y)[28,29] was 1.24 x [10.sup.-6]--which was very similar to that reported for mesothelioma in the literature. Given that no substantial difference was found between mesothelioma mortality in Taiwan and mortality reported in the literature, we simply applied the rate to assess the excess numbers of mesothelioma for the individuals in Taiwan. We adopted Peto's model for asbestos-related mesothelioma[30,31]; in that model, mesothelioma is assumed to be independent of smoking and associated to duration since initial exposure (with an order of 3.2-4.0). The model is as follows:

I(t) = K x C ([T.sup.3.2] - [T - D)[sup.3.2])

0 [is less than] T [is less than] D

I(t) = K x C x [T.sup.3.2]

T [is greater than] D,